We are searching data for your request:
Upon completion, a link will appear to access the found materials.
When scientists choose viruses for the influenza vaccine based on biological and clinical data, what indicates that a certain strain will circulate and likely be dominant in a certain season?
Does a low HI titer (meaning antigenic novelty) for a virus antigen relative to an antiserum of a virus that is currently prevalent mean that the new virus will likely dominate in the next season? OR is a high HI titer a better choice for the vaccine since it means the virus in question is very similar to currently circulating viruses?
Again, the full answer is too complex to answer here. The CDC has a broad explanation (Selecting Viruses for the Seasonal Influenza Vaccine) and the WHO has a presentation summarizing the process (The WHO Vaccine Strain Selection Process: Review of the Evidence).
The major factor for choosing a new vaccine virus is based on surveillance from the preceding season and from the opposite hemisphere's season. The surveillance data shows which virus groups are expanding or shrinking. Antigenic variation (high or low HI titers) is also a part of the decision, but every season has a number of viruses that have low HI titers to the current vaccine and the real question is whether those occasional outliers are just sporadic, or whether they're showing signs of becoming increasingly common.
Interpreting whether particular virus families are increasing or not requires a lot of familiarity with influenza behavior, genetics, and antigenicity. You can look at some of the data used in strain selection on the WHO site, e.g. Recommended composition of influenza virus vaccines for use in the 2018- 2019 northern hemisphere influenza season.
Targeting the Achilles’ Heel of Influenza Viruses
Influenza viruses are ingenious at evading our body’s natural immune system defenses by constantly mutating, allowing these viruses to re-emerge year after year. Genentech scientists are exploring a new way to fight back.
February 18, 2014 – Every year in the United States, 5-20% of the population becomes ill with the flu (influenza). Vaccination is the best way to reduce the chance you’ll catch seasonal flu and spread it to others. But due to constant changes in the flu viruses circulating worldwide, annual vaccination is necessary. This diversity in flu viruses makes fighting the flu a big challenge. Let me explain how the flu evades our immune system defenses, and what Genentech scientists are trying to do about it.
Two broad types of flu virus can cause severe illness in humans: A and B.
Influenza A is of greatest concern because it not only causes seasonal flu, but is also responsible for worldwide pandemics.
Influenza B doesn’t have as much genetic diversity as influenza A, and thus isn’t a pandemic threat. But influenza B still causes severe disease in the very young, especially premature infants, the immune compromised and the elderly.
Importantly, both virus types are included in the seasonal flu vaccine.
The Influenza viruses section of Virology Journal will publish articles on all aspects of influenza virus research, including molecular genetics, molecular biology, biochemistry, biophysics, structural biology, cell biology, immunology, morphology, and pathogenesis. The section will also welcome the case reports of influenza outbreaks in both human and animal populations, and development and evaluation of vaccines and antiviral compounds in humans and animals.
Avian influenza virus H9N2 infections in farmed minks
The prevalence of avian H9N2 viruses throughout Asia, along with their demonstrated ability to infect mammals, puts them high on the list of influenza viruses with pandemic potential for humans. In this study.
Authors: Chuanmei Zhang, Yang Xuan, Hu Shan, Haiyan Yang, Jianlin Wang, Ke Wang, Guimei Li and Jian Qiao
Citation: Virology Journal 2015 12 :180
Published on: 2 November 2015
Throat and nasal swabs for molecular detection of respiratory viruses in acute pharyngitis
Detection of specific respiratory viruses is important for surveillance programs, where nasopharyngeal or nasal swabs have traditionally been used. Our objective was to determine whether sampling with a throat.
Authors: Mohsin Ali, Sangsu Han, Chris J. Gunst, Steve Lim, Kathy Luinstra and Marek Smieja
Citation: Virology Journal 2015 12 :178
Content type: Short report
Published on: 29 October 2015
Intranasal administration of poly-gamma glutamate induced antiviral activity and protective immune responses against H1N1 influenza A virus infection
The global outbreak of a novel swine-origin strain of the 2009 H1N1 influenza A virus and the sudden, worldwide increase in oseltamivir-resistant H1N1 influenza A viruses highlight the urgent need for novel an.
Authors: Eun-Ha Kim, Young-Ki Choi, Chul-Joong Kim, Moon-Hee Sung and Haryoung Poo
Citation: Virology Journal 2015 12 :160
Published on: 6 October 2015
Wild bird surveillance for highly pathogenic avian influenza H5 in North America
It is unknown how the current Asian origin highly pathogenic avian influenza H5 viruses arrived, but these viruses are now poised to become endemic in North America. Wild birds harbor these viruses and have di.
Authors: Paul L. Flint, John M. Pearce, J. Christian Franson and Dirk V. Derksen
Citation: Virology Journal 2015 12 :151
Published on: 28 September 2015
Reverse-transcription, loop-mediated isothermal amplification assay for the sensitive and rapid detection of H10 subtype avian influenza viruses
The H10 subtype avian influenza viruses (H10N4, H10N5 and H10N7) have been reported to cause disease in mammals, and the first human case of H10N8 subtype avian influenza virus was reported in 2013. Recently, .
Authors: Sisi Luo, Zhixun Xie, Liji Xie, Jiabo Liu, Zhiqin Xie, Xianwen Deng, Li Huang, Jiaoling Huang, Tingting Zeng and Mazhar I. Khan
Citation: Virology Journal 2015 12 :145
Published on: 17 September 2015
Protective efficacy of an inactivated vaccine against H9N2 avian influenza virus in ducks
Wild ducks play an important role in the evolution of avian influenza viruses (AIVs). Domestic ducks in China are known to carry and spread H9N2 AIVs that are thought to have contributed internal genes for the.
Authors: Qiaoyang Teng, Weixia Shen, Qinfang Liu, Guangyu Rong, Lin Chen, Xuesong Li, Hongjun Chen, Jianmei Yang and Zejun Li
Citation: Virology Journal 2015 12 :143
Content type: Short report
Published on: 17 September 2015
Viral dominance of reassortants between canine influenza H3N2 and pandemic (2009) H1N1 viruses from a naturally co-infected dog
Since avian-origin H3N2 canine influenza virus (CIV) was first identified in South Korea in 2008, the novel influenza virus has been reported in several countries in Asia. Reverse zoonotic transmission of pand.
Authors: Woonsung Na, Kwang-Soo Lyoo, Eun-jung Song, Minki Hong, Minjoo Yeom, Hyoungjoon Moon, Bo-Kyu Kang, Doo-Jin Kim, Jeong-Ki Kim and Daesub Song
Citation: Virology Journal 2015 12 :134
Content type: short report
Published on: 4 September 2015
Identification of putative interactions between swine and human influenza A virus nucleoprotein and human host proteins
Influenza A viruses (IAVs) are important pathogens that affect the health of humans and many additional animal species. IAVs are enveloped, negative single-stranded RNA viruses whose genome encodes at least te.
Authors: Alex Generous, Molly Thorson, Jeff Barcus, Joseph Jacher, Marc Busch and Heidi Sleister
Citation: Virology Journal 2014 11 :228
Published on: 30 December 2014
Sampling variability between two mid-turbinate swabs of the same patient has implications for influenza viral load monitoring
With the clinical development of several antiviral intervention strategies for influenza, it becomes crucial to explore viral load shedding in the nasal cavity as a biomarker for treatment success, but also to.
Authors: Liesbeth Van Wesenbeeck, Hanne Meeuws, David D’Haese, Gabriela Ispas, Lieselot Houspie, Marc Van Ranst and Lieven J Stuyver
Citation: Virology Journal 2014 11 :233
Content type: Short report
Published on: 24 December 2014
Combination of specific single chain antibody variable fragment and siRNA has a synergistic inhibitory effect on the propagation of avian influenza virus H5N1 in chicken cells
The avian influenza virus (AIV) causes frequent disease with high morbidity and mortality. RNA interference (RNAi) has been shown to provide an effective antiviral defense in animals, and several studies have .
Authors: Shuang Wang, Peng Zhang, Fei He, Ji-Gui Wang, Jia-Zeng Sun, Zhi-Li Li, Bao Yi, Ji Xi, Ya-Ping Mao, Qiang Hou, Dao-Li Yuan, Zi-Ding Zhang and Wei-Quan Liu
Citation: Virology Journal 2014 11 :208
Published on: 29 November 2014
The pathogenicity of swan derived H5N1 virus in birds and mammals and its gene analysis
Highly pathogenic avian influenza (HPAI) H5N1 viruses continue to circulate in poultry and can infect and cause mortality in birds and mammals the genetic determinants of their increased virulence are largely.
Authors: Kairat Tabynov, Abylay Sansyzbay, Nurlan Sandybayev and Muratbay Mambetaliyev
Citation: Virology Journal 2014 11 :207
Published on: 29 November 2014
Molecular characterization of H3N2 influenza A viruses isolated from Ontario swine in 2011 and 2012
Data about molecular diversity of commonly circulating type A influenza viruses in Ontario swine are scarce. Yet, this information is essential for surveillance of animal and public health, vaccine updates, an.
Authors: Helena Grgić, Marcio Costa, Robert M Friendship, Susy Carman, Éva Nagy, Greg Wideman, Scott Weese and Zvonimir Poljak
Citation: Virology Journal 2014 11 :194
Published on: 22 November 2014
Transmission of H7N9 influenza virus in mice by different infective routes
On 19 February 2013, the first patient infected with a novel influenza A H7N9 virus from an avian source showed symptoms of sickness. More than 349 laboratory-confirmed cases and 109 deaths have been reported .
Authors: Linlin Bao, Lili Xu, Hua Zhu, Wei Deng, Ting Chen, Qi Lv, Fengdi Li, Jing Yuan, Yanfeng Xu, Lan Huang, Yanhong Li, Jiangning Liu, Yanfeng Yao, Pin Yu, Honglin Chen and Chuan Qin
Citation: Virology Journal 2014 11 :185
Published on: 3 November 2014
Comparative pathology of pigs infected with Korean H1N1, H1N2, or H3N2 swine influenza A viruses
The predominant subtypes of swine influenza A virus (SIV) in Korea swine population are H1N1, H1N2, and H3N2. The viruses are genetically close to the classical U.S. H1N1 and triple-reassortant H1N2 and H3N2 v.
Authors: Kwang-Soo Lyoo, Jeong-Ki Kim, Kwonil Jung, Bo-Kyu Kang and Daesub Song
Citation: Virology Journal 2014 11 :170
Content type: Short report
Published on: 24 September 2014
Identification of swine influenza virus epitopes and analysis of multiple specificities expressed by cytotoxic T cell subsets
Major histocompatibility complex (MHC) class I peptide binding and presentation are essential for antigen-specific activation of cytotoxic T lymphocytes (CTLs) and swine MHC class I molecules, also termed swin.
Authors: Lasse E Pedersen, Solvej Ø Breum, Ulla Riber, Lars E Larsen and Gregers Jungersen
Citation: Virology Journal 2014 11 :163
Content type: Short report
Published on: 6 September 2014
An efficient genome sequencing method for equine influenza [H3N8] virus reveals a new polymorphism in the PA-X protein
H3N8 equine influenza virus (EIV) has caused disease outbreaks in horses across the world since its first isolation in 1963. However, unlike human, swine and avian influenza, there is relatively little sequenc.
Authors: Adam Rash, Alana Woodward, Neil Bryant, John McCauley and Debra Elton
Citation: Virology Journal 2014 11 :159
Published on: 2 September 2014
Influenza polymerase encoding mRNAs utilize atypical mRNA nuclear export
Influenza is a segmented negative strand RNA virus. Each RNA segment is encapsulated by influenza nucleoprotein and bound by the viral RNA dependent RNA polymerase (RdRP) to form viral ribonucleoproteins respo.
Authors: Sean Larsen, Steven Bui, Veronica Perez, Adeba Mohammad, Hilario Medina-Ramirez and Laura L Newcomb
Citation: Virology Journal 2014 11 :154
Published on: 28 August 2014
Mutations within the conserved NS1 nuclear export signal lead to inhibition of influenza A virus replication
The influenza A virus NS1 protein is a virulence factor and an antagonist of host cell innate immune responses. During virus infection NS1 protein has several functions both in the nucleus and in the cytoplasm.
Authors: Janne Tynell, Krister Melén and Ilkka Julkunen
Citation: Virology Journal 2014 11 :128
Published on: 14 July 2014
Pandemic clinical case definitions are non-specific: multiple respiratory viruses circulating in the early phases of the 2009 influenza pandemic in New South Wales, Australia
During the early phases of the 2009 pandemic, subjects with influenza-like illness only had laboratory testing specific for the new A(H1N1)pdm09 virus.
Authors: Vigneswary Mala Ratnamohan, Janette Taylor, Frank Zeng, Kenneth McPhie, Christopher C Blyth, Sheena Adamson, Jen Kok and Dominic E Dwyer
Citation: Virology Journal 2014 11 :113
Content type: Short report
Published on: 18 June 2014
Membrane-bound IL-12 and IL-23 serve as potent mucosal adjuvants when co-presented on whole inactivated influenza vaccines
Potent and safe adjuvants are needed to improve the efficacy of parenteral and mucosal vaccines. Cytokines, chemokines and growth factors have all proven to be effective immunomodulatory adjuvants when adminis.
Authors: Tila Khan, Connie L Heffron, Kevin P High and Paul C Roberts
Citation: Virology Journal 2014 11 :78
Content type: Short report
Phylogenetic and antigenic characterization of reassortant H9N2 avian influenza viruses isolated from wild waterfowl in the East Dongting Lake wetland in 2011–2012
Wild waterfowl are recognized as the natural reservoir for influenza A viruses. Two distinct lineages, the American and Eurasian lineages, have been identified in wild birds. Gene flow between the two lineages.
Authors: Yun Zhu, Shixiong Hu, Tian Bai, Lei Yang, Xiang Zhao, Wenfei Zhu, Yiwei Huang, Zhihong Deng, Hong Zhang, Zhiyong Bai, Mingdong Yu, Jianfei Huang and Yuelong Shu
Citation: Virology Journal 2014 11 :77
Published on: 30 April 2014
H5-based DNA constructs derived from selected highly pathogenic H5N1 avian influenza virus induce high levels of humoral antibodies in Muscovy ducks against low pathogenic viruses
H5 low pathogenic avian influenza virus (LPAIV) infection in domestic ducks is a major problem in duck producing countries. Their silent circulation is an ongoing source of potential highly pathogenic or zoono.
Authors: Olivier Guionie, Éric Niqueux, Michel Amelot, Stéphanie Bougeard and Véronique Jestin
Citation: Virology Journal 2014 11 :74
Content type: Short report
Published on: 24 April 2014
Hyperimmune intravenous immunoglobulin containing high titers of pandemic H1N1 hemagglutinin and neuraminidase antibodies provides dose-dependent protection against lethal virus challenge in SCID mice
Convalescent plasma and fractionated immunoglobulins have been suggested as prophylactic or therapeutic interventions during an influenza pandemic.
Authors: Christine Hohenadl, Walter Wodal, Astrid Kerschbaum, Richard Fritz, M Keith Howard, Maria R Farcet, Daniel Portsmouth, John K McVey, Donald A Baker, Hartmut J Ehrlich, P Noel Barrett and Thomas R Kreil
Citation: Virology Journal 2014 11 :70
Content type: Short report
Published on: 16 April 2014
Influenza viral vectors expressing the Brucella OMP16 or L7/L12 proteins as vaccines against B. abortus infection
We generated novel, effective candidate vaccine against Brucella abortus based on recombinant influenza viruses expressing the Brucella ribosomal protein L7/L12 or outer membrane protein (Omp)-16 from the NS1 ope.
Authors: Kaissar Tabynov, Abylai Sansyzbay, Zhailaubay Kydyrbayev, Bolat Yespembetov, Sholpan Ryskeldinova, Nadezhda Zinina, Nurika Assanzhanova, Kulaisan Sultankulova, Nurlan Sandybayev, Berik Khairullin, Irina Kuznetsova, Boris Ferko and Andrej Egorov
Citation: Virology Journal 2014 11 :69
Published on: 10 April 2014
Kinetics of pulmonary immune cells, antibody responses and their correlations with the viral clearance of influenza A fatal infection in mice
Fatal influenza A virus infection is a major threat to public health throughout the world. Lung macrophages and neutrophils have critical roles for both the pathogenesis and viral clearance of fatal viral infe.
Authors: Jin Lv, Yanhong Hua, Dan Wang, Aofei Liu, Juan An, Aimin Li, Yanfeng Wang, Xiliang Wang, Na Jia and Qisheng Jiang
Citation: Virology Journal 2014 11 :57
Published on: 26 March 2014
Serological report of pandemic (H1N1) 2009 infection among cats in Northeastern China in 2012-02 and 2013-03
Influenza A virus has a wide range of hosts. It has not only infected human, but also been reported interspecies transmission from humans to other animals, such as pigs, poultry, dogs and cats. However, preval.
Authors: Fu-Rong Zhao, Chun-Guo Liu, Xin Yin, Dong-Hui Zhou, Ping Wei and Hui-Yun Chang
Citation: Virology Journal 2014 11 :49
Content type: Short report
Published on: 14 March 2014
Viral aetiology influenza like illnesses in Santa Cruz, Bolivia (2010–2012)
Acute respiratory infections represent a serious public health issue worldwide but virological aetiologies of Influenza Like Illnesses (ILIs) remain largely unknown in developing countries. This study represen.
Authors: Julie Delangue, Yelin Roca Sanchez, Géraldine Piorkowski, Maël Bessaud, Cécile Baronti, Laurence Thirion-Perrier, Roxana Loayza Mafayle, Cinthia Avila Ardaya, Gabriela Añez Aguilera, Jimmy Revollo Guzman, Javier Lora Riera and Xavier de Lamballerie
Citation: Virology Journal 2014 11 :35
Published on: 24 February 2014
Heterosubtypic protective immunity against widely divergent influenza subtypes induced by fusion protein 4sM2 in BALB/c mice
Regular reformulation of currently available vaccines is necessary due to the unpredictable variability of influenza viruses. Therefore, vaccine based on a highly conserved antigen with capability of induction.
Authors: Mohammed YE Chowdhury, Soo-Kyung Seo, Ho-Jin Moon, Melbourne R Talactac, Jae-Hoon Kim, Min-Eun Park, Hwa-Young Son, Jong-Soo Lee and Chul-Joong Kim
Citation: Virology Journal 2014 11 :21
Published on: 6 February 2014
Seroprevalence Survey of Avian influenza A (H5) in wild migratory birds in Yunnan Province, Southwestern China
Highly pathogenic avian influenza virus (HPAIV) is a highly contagious disease which is a zoonotic pathogen of significant economic and public health concern. The outbreaks caused by HPAIV H5N1 of Asian origin.
Authors: Hua Chang, Feiyan Dai, Zili Liu, Feizhou Yuan, Siyue Zhao, Xun Xiang, Fengcai Zou, Bangquan Zeng, YaTing Fan and Gang Duan
Citation: Virology Journal 2014 11 :18
Published on: 3 February 2014
Determinants of individuals’ risks to 2009 pandemic influenza virus infection at household level amongst Djibouti city residents - A CoPanFlu cross-sectional study
Following the 2009 swine flu pandemic, a cohort for pandemic influenza (CoPanFlu) study was established in Djibouti, the Horn of Africa, to investigate its case prevalence and risk predictors’ at household level.
Authors: Fred Andayi, Pascal Crepey, Alexia Kieffer, Nicolas Salez, Ammar A Abdo, Fabrice Carrat, Antoine Flahault and Xavier de Lamballerie
Citation: Virology Journal 2014 11 :13
Published on: 27 January 2014
Thank you to Virology Journal's peer reviewers in 2013
The editors of Virology Journal would like to thank all our reviewers who have contributed to the journal in Volume 10 (2013). The success of any scientific journal depends on an effective and strict peer review .
Citation: Virology Journal 2014 11 :4
Content type: Reviewer acknowledgement
Published on: 22 January 2014
Genetic mutations in influenza H3N2 viruses from a 2012 epidemic in Southern China
An influenza H3N2 epidemic occurred throughout Southern China in 2012.
Authors: Jing Zhong, Lijun Liang, Ping Huang, Xiaolan Zhu, Lirong Zou, Shouyi Yu, Xin Zhang, Yonghui Zhang, Hanzhong Ni and Jin Yan
Citation: Virology Journal 2013 10 :345
Published on: 26 November 2013
Influenza A penetrates host mucus by cleaving sialic acids with neuraminidase
Influenza A virus (IAV) neuraminidase (NA) cleaves sialic acids (Sias) from glycans. Inhibiting NA with oseltamivir suppresses both viral infection, and viral release from cultured human airway epithelial cell.
Authors: Miriam Cohen, Xing-Quan Zhang, Hooman P Senaati, Hui-Wen Chen, Nissi M Varki, Robert T Schooley and Pascal Gagneux
Citation: Virology Journal 2013 10 :321
Published on: 22 November 2013
Transcription factor regulation and cytokine expression following in vitro infection of primary chicken cell culture with low pathogenic avian influenza virus
Avian influenza virus (AIV) induced proinflammatory cytokine expression is believed to contribute to the disease pathogenesis following infection of poultry. However, there is limited information on the avian .
Authors: Haijun Jiang, Kangzhen Yu and Darrell R Kapczynski
Citation: Virology Journal 2013 10 :342
Published on: 19 November 2013
Survey of causative agents for acute respiratory infections among patients in Khartoum- State, Sudan, 2010–2011
This study was carried out to determine causative agents of acute respiratory illness of patients in Khartoum State, Sudan.
Authors: Khalid A Enan, Takeshi Nabeshima, Toru Kubo, Corazon C Buerano, Abdel Rahim M El Hussein, Isam M Elkhidir, Eltahir AG Khalil and Kouichi Morita
Citation: Virology Journal 2013 10 :312
Published on: 25 October 2013
H9N2 avian influenza infection altered expression pattern of Sphiogosine-1-phosphate Receptor 1 in BALB/c mice
The pathological damage inflicted by virulent AIV strains is often caused by inducing a positive feedback loop of cytokines in immune cells that cause excessive inflammation. Previous research has shown that a.
Authors: Shuang Tong, Jin Tian, Heng Wang, Zhiqiang Huang, Meng Yu, Lingshuang Sun, Rongchang Liu, Ming Liao and Zhangyong Ning
Citation: Virology Journal 2013 10 :296
Published on: 30 September 2013
Cross-protective immunity against influenza A/H1N1 virus challenge in mice immunized with recombinant vaccine expressing HA gene of influenza A/H5N1 virus
Influenza virus undergoes constant antigenic evolution, and therefore influenza vaccines must be reformulated each year. Time is necessary to produce a vaccine that is antigenically matched to a pandemic strai.
Authors: Song Yang, Shumeng Niu, Zhihua Guo, Ye Yuan, Kun Xue, Sinan Liu and Hong Jin
Citation: Virology Journal 2013 10 :291
Published on: 22 September 2013
Genetic and biological characterisation of an avian-like H1N2 swine influenza virus generated by reassortment of circulating avian-like H1N1 and H3N2 subtypes in Denmark
The influenza A virus subtypes H1N1, H1N2 and H3N2 are the most prevalent subtypes in swine. In 2003, a reassorted H1N2 swine influenza virus (SIV) subtype appeared and became prevalent in Denmark. In the pres.
Authors: Ramona Trebbien, Karoline Bragstad, Lars Erik Larsen, Jens Nielsen, Anette Bøtner, Peter MH Heegaard, Anders Fomsgaard, Birgitte Viuff and Charlotte Kristiane Hjulsager
Citation: Virology Journal 2013 10 :290
Published on: 18 September 2013
Inactivation of the novel avian influenza A (H7N9) virus under physical conditions or chemical agents treatment
In the spring of 2013, a novel avian-origin influenza A (H7N9) virus in Eastern China emerged causing human infections. Concerns that a new influenza pandemic could occur were raised. The potential effect of c.
Authors: Shumei Zou, Junfeng Guo, Rongbao Gao, Libo Dong, Jianfang Zhou, Ye Zhang, Jie Dong, Hong Bo, Kun Qin and Yuelong Shu
Citation: Virology Journal 2013 10 :289
Published on: 15 September 2013
High resolution melting analysis: rapid and precise characterisation of recombinant influenza A genomes
High resolution melting analysis (HRM) is a rapid and cost-effective technique for the characterisation of PCR amplicons. Because the reverse genetics of segmented influenza A viruses allows the generation of .
Authors: Donata Kalthoff, Martin Beer and Bernd Hoffmann
Citation: Virology Journal 2013 10 :284
Published on: 12 September 2013
Rapid emergence of a virulent PB2 E627K variant during adaptation of highly pathogenic avian influenza H7N7 virus to mice
Highly pathogenic avian influenza (HPAI) viruses pose a potential human health threat as they can be transmitted directly from infected poultry to humans. During a large outbreak of HPAI H7N7 virus among poult.
Authors: Rineke MC de Jong, Norbert Stockhofe-Zurwieden, Eline S Verheij, Els A de Boer-Luijtze, Saskia JM Ruiter, Olav S de Leeuw and Lisette AHM Cornelissen
Citation: Virology Journal 2013 10 :276
Published on: 5 September 2013
The mouse and ferret models for studying the novel avian-origin human influenza A (H7N9) virus
The current study was conducted to establish animal models (including mouse and ferret) for the novel avian-origin H7N9 influenza virus.
Authors: Lili Xu, Linlin Bao, Wei Deng, Hua Zhu, Ting Chen, Qi Lv, Fengdi Li, Jing Yuan, Zhiguang Xiang, Kai Gao, Yanfeng Xu, Lan Huang, Yanhong Li, Jiangning Liu, Yanfeng Yao, Pin Yu&hellip
Citation: Virology Journal 2013 10 :253
Content type: Short report
Published on: 8 August 2013
The Correction to this article has been published in Virology Journal 2020 17:83
Distinction of subtype-specific antibodies against European porcine influenza viruses by indirect ELISA based on recombinant hemagglutinin protein fragment-1
Serological investigations of swine influenza virus infections and epidemiological conclusions thereof are challenging due to the complex and regionally variable pattern of co-circulating viral subtypes and li.
Authors: Na Zhao, Elke Lange, Sybille Kubald, Christian Grund, Martin Beer and Timm C Harder
Citation: Virology Journal 2013 10 :246
Published on: 30 July 2013
Cross-reactive human B cell and T cell epitopes between influenza A and B viruses
Influenza A and B viruses form different genera, which were originally distinguished by antigenic differences in their nucleoproteins and matrix 1 proteins. Cross-protection between these two genera has not be.
Authors: Masanori Terajima, Jenny Aurielle B Babon, Mary Dawn T Co and Francis A Ennis
Citation: Virology Journal 2013 10 :244
Published on: 26 July 2013
Influenza A/Hong Kong/156/1997(H5N1) virus NS1 gene mutations F103L and M106I both increase IFN antagonism, virulence and cytoplasmic localization but differ in binding to RIG-I and CPSF30
The genetic basis for avian to mammalian host switching in influenza A virus is largely unknown. The human A/HK/156/1997 (H5N1) virus that transmitted from poultry possesses NS1 gene mutations F103L + M106I th.
Authors: Samar K Dankar, Elena Miranda, Nicole E Forbes, Martin Pelchat, Ali Tavassoli, Mohammed Selman, Jihui Ping, Jianjun Jia and Earl G Brown
Citation: Virology Journal 2013 10 :243
Published on: 25 July 2013
Surveillance on A/H5N1 virus in domestic poultry and wild birds in Egypt
The endemic H5N1 high pathogenicity avian influenza virus (A/H5N1) in poultry in Egypt continues to cause heavy losses in poultry and poses a significant threat to human health.
Authors: Elham F El-Zoghby, Mona M Aly, Soad A Nasef, Mohamed K Hassan, Abdel-Satar Arafa, Abdullah A Selim, Shereen G Kholousy, Walid H Kilany, Marwa Safwat, E M Abdelwhab and Hafez M Hafez
A Live Attenuated Influenza Vaccine Elicits Enhanced Heterologous Protection When the Internal Genes of the Vaccine Are Matched to Those of the Challenge Virus
Influenza A virus (IAV) causes significant morbidity and mortality, despite the availability of viral vaccines. The efficacy of live attenuated influenza vaccines (LAIVs) has been especially poor in recent years. One potential reason is that the master donor virus (MDV), on which all LAIVs are based, contains either the internal genes of the 1960 A/Ann Arbor/6/60 or the 1957 A/Leningrad/17/57 H2N2 viruses (i.e., they diverge considerably from currently circulating strains). We previously showed that introduction of the temperature-sensitive (ts) residue signature of the AA/60 MDV into a 2009 pandemic A/California/04/09 H1N1 virus (Cal/09) results in only 10-fold in vivo attenuation in mice. We have previously shown that the ts residue signature of the Russian A/Leningrad/17/57 H2N2 LAIV (Len LAIV) more robustly attenuates the prototypical A/Puerto Rico/8/1934 (PR8) H1N1 virus. In this work, we therefore introduced the ts signature from Len LAIV into Cal/09. This new Cal/09 LAIV is ts in vitro, highly attenuated (att) in mice, and protects from a lethal homologous challenge. In addition, when our Cal/09 LAIV with PR8 hemagglutinin and neuraminidase was used to vaccinate mice, it provided enhanced protection against a wild-type Cal/09 challenge relative to a PR8 LAIV with the same attenuating mutations. These findings suggest it may be possible to improve the efficacy of LAIVs by better matching the sequence of the MDV to currently circulating strains.IMPORTANCE Seasonal influenza infection remains a major cause of disease and death, underscoring the need for improved vaccines. Among current influenza vaccines, the live attenuated influenza vaccine (LAIV) is unique in its ability to elicit T-cell immunity to the conserved internal proteins of the virus. Despite this, LAIV has shown limited efficacy in recent years. One possible reason is that the conserved, internal genes of all current LAIVs derive from virus strains that were isolated between 1957 and 1960 and that, as a result, do not resemble currently circulating influenza viruses. We have therefore developed and tested a new LAIV, based on a currently circulating pandemic strain of influenza. Our results show that this new LAIV elicits improved protective immunity compared to a more conventional LAIV.
Keywords: IIV LAIV MDV heterologous immunity and protection inactivated influenza vaccine influenza live attenuated influenza vaccine master donor virus.
Copyright © 2020 Smith et al.
Cal/09 Len has a more robust ts phenotype than Cal/09 AA. (A) Schematic…
Attenuation of Cal/09Len and Cal/09AA…
Attenuation of Cal/09Len and Cal/09AA in mice. Mice (see Materials and Methods) were…
Cal/09 Len replicates at lower…
Cal/09 Len replicates at lower levels in vivo than Cal/09 AA but still…
Cal/09 Len protects mice from…
Cal/09 Len protects mice from a lethal homologous challenge at safe doses. Mice…
Cal/09 Len confers better protection…
Cal/09 Len confers better protection against a lethal heterologous challenge than PR8/Len. Mice…
Enhanced heterologous protection conferred by…
Enhanced heterologous protection conferred by Cal/09 Len is T cell mediated. (A) Cal/09…
Depleting antibodies effectively diminish T-cell…
Depleting antibodies effectively diminish T-cell subsets. Cells from lungs (top row), MLNs (middle…
Innate Immune Evasion Strategies of Influenza Viruses
The currently circulating swine-origin H1N1 pandemic influenza A virus provided somewhat of a surprise to the research community, who were focused on highly pathogenic avian viruses in poultry. This new virus appears to have already caused significant morbidity and mortality worldwide, and is clearly an ongoing public health concern that will occupy our focus for the near future. The immediate priority must be to monitor the evolution of this pandemic virus in order to assess whether it acquires known virulence determinants. Of course, the development of effective countermeasures (such as protective vaccines) to combat the consequences of human infection is essential. The technical abilities that we have as a scientific community, combined with the rapid response of many laboratories, means that now more than ever we are well positioned to deal effectively with this virus.
From a purely research point of view, the swine-origin H1N1 virus is likely to provide interesting insights into how pandemic influenza viruses are generated. Data from whole-genome sequencing efforts, together with 'real-time' in vivo and in vitro laboratory studies (which will be essential for monitoring any virulence changes in this virus) should give us a better understanding of how influenza viruses adapt to new species, and what the barriers to species–species 'jumps' are. Identification of the precursor to this emergent pandemic virus, which has presumably circulated in pigs for some time, will obviously be necessary.
We already have some idea that the host innate immune response can be a significant restriction to influenza viruses adapted to an alternative host.  Indeed, avian and human influenza viruses exhibit differential susceptibility to the IFN-inducible mouse Mx1 and human MxA antiviral proteins.  Furthermore, it is unclear why highly pathogenic H5N1 influenza viruses replicate poorly and cause mild disease in swine,  yet are highly virulent in mice, chickens, ferrets and macaques. Similarly, the reconstructed 1918 pandemic influenza virus causes moderate pulmonary pathology in swine,  but induces a fatal disease course in mice, ferrets and macaques. [25,198,199] Even more remarkable is the complete lack of virulence of both highly pathogenic H5N1 influenza viruses and the reconstructed 1918 pandemic influenza virus in guinea pigs, despite the high levels of virus replication in the respiratory tract.  Overall, this suggests that there is a major host component to pathogenicity. Thus, we still need to understand the molecular changes required by a virus to allow it to circumvent particular host-specific responses. Following on from this, most current research into innate immune processes and viral countermeasures is biased towards human model systems, and future work could also address how these virus–host interactions work in other species. From a practical point of view, this may be particularly important for animal vaccine development and antiviral drug design. From a comparative biology point of view, such studies will continue to help us uncover how normal cellular processes work.
For antivirals, it is clear that a number of alternative strategies are currently being pursued and are at various stages of development (reviewed in  ). A molecular understanding of the structural mechanics of influenza virus replication (and not least the interaction of viral proteins with cellular factors) is likely to drive the discovery and validation of new antiviral targets. As soon as a library of these new drugs becomes licensed for use in humans, our ability to control outbreaks of potentially prepandemic influenza viruses will increase, particularly with the use of ever-changing combination therapies.
A step toward a universal flu vaccine
Transmission electron micrograph of influenza A virus, late passage. Credit: CDC
Each year, the flu vaccine has to be redesigned to account for mutations that the virus accumulates, and even then, the vaccine is often not fully protective for everyone.
Researchers at MIT and the Ragon Institute of MIT, MGH, and Harvard are now working on strategies for designing a universal flu vaccine that could work against any flu strain. In a new study, they describe a vaccine that triggers an immune response against an influenza protein segment that rarely mutates but is normally not targeted by the immune system.
The vaccine consists of nanoparticles coated with flu proteins that train the immune system to create the desired antibodies. In studies of mice with humanized immune systems, the researchers showed that their vaccine can elicit an antibody response targeting that elusive protein segment, raising the possibility that the vaccine could be effective against any flu strain.
"The reason we're excited about this work is that it is a small step toward developing a flu shot that you just take once, or a few times, and the resulting antibody response is likely to protect against seasonal flu strains and pandemic strains as well," says Arup K. Chakraborty, the Robert T. Haslam Professor in Chemical Engineering and professor of physics and chemistry at MIT, and a member of MIT's Institute for Medical Engineering and Science and the Ragon Institute of MGH, MIT, and Harvard.
Chakraborty and Daniel Lingwood, an assistant professor at Harvard Medical School and a group leader at the Ragon Institute, are the senior authors of the study, which appears in Cell Systems. MIT research scientist Assaf Amitai is the lead author of the paper.
Most flu vaccines consist of inactivated flu viruses. These viruses are coated with a protein called hemagglutinin (HA), which helps them bind to host cells. After vaccination, the immune system generates squadrons of antibodies that target the HA protein. These antibodies almost always bind to the head of the HA protein, which is the part of the protein that mutates the most rapidly. Parts of the HA stem, on the other hand, very rarely mutate.
"We don't understand the complete picture yet, but for many reasons, the immune system is intrinsically not good at seeing the conserved parts of these proteins, which if effectively targeted would elicit an antibody response that would neutralize multiple influenza types," Lingwood says.
In their new study, the researchers set out to study why the immune system ends up targeting the HA head rather than the stem, and to find ways to refocus the immune system's attention on the stem. Such a vaccine could elicit antibodies known as "broadly neutralizing antibodies," which would respond to any flu strain. In principle, this kind of vaccine could end the arms race between vaccine designers and rapidly mutating flu viruses.
One factor that was already known to contribute to antibody preference for the HA head is that HA proteins are densely clustered on the surface of the virus, so it's difficult for antibodies to access the stem region. The head region is much more accessible.
The researchers developed a computational model that helped them to further explore the "immunodominance" of the protein's head region. "We hypothesized that the surface geometry of the virus could be key to its ability to survive by protecting its vulnerable parts from antibodies," Amitai says.
The researchers explored the effects of geometry on immunodominance using a technique called molecular dynamics simulation. They further modeled a process called antibody affinity maturation. This process, which occurs after B cells encounter a virus (or a vaccine), determines which antibodies will predominate during the immune response.
Each B cell has on its surface proteins called B cell receptors, which bind to different foreign proteins. Once a particular B cell receptor binds strongly to the HA protein, that B cell becomes activated and starts to multiply rapidly. This process introduces new mutations into the B cell receptors, some of which bind more strongly. These better binders tend to survive, while the weaker binders die. At the end of this process, which takes one or two weeks, there is a population of B cells that is very good at binding strongly to the HA protein. These B cells secrete antibodies that bind to the HA protein.
"As time goes on, after infection, the antibodies get better and better at targeting this particular antigen," Chakraborty says.
The researchers' computer simulations of this process revealed that when a typical flu vaccine is given, B cell receptors that bind strongly to the HA stem are at a competitive disadvantage during the maturation process, because they can't reach their targets as easily as B cell receptors that bind strongly to the HA head.
The researchers also used their computer model to simulate this maturation process with a nanoparticle vaccine developed at the National Institutes of Health, which is now in a phase 1 clinical trial. This particle carries HA stem proteins spaced out at lower density. The model showed that this arrangement makes the proteins more accessible to antibodies, which are Y-shaped, allowing the antibodies to grab onto the proteins with both arms. The simulations revealed that those stem-targeting antibodies predominated at the end of the maturation process.
The researchers also used their computational model to predict the outcome of several possible vaccination strategies. One strategy that appears promising is to immunize with an HA stem from a virus that is similar to, but not the same as, strains that the recipient has previously been exposed to. In 2009, many people around the world were either infected with or vaccinated against a novel H1N1 strain. The modeling led the researchers to hypothesize that if they vaccinated with nanoparticles displaying HA-like proteins from a strain that is different from the 2009 version, it should elicit the kind of broadly neutralizing antibodies that may confer universal immunity.
Using mice with human immune cells, the researchers tested this strategy, first immunizing them against the 2009 H1N1 strain, followed by a nanoparticle vaccine carrying the HA stem protein from a different H1N1 strain. They found that this approach was much more successful at eliciting broadly neutralizing antibodies than any of the other strategies that they tested.
"We discovered that this particular event in our immune history can actually be harnessed with this particular nanoparticle to refocus the immune system's attention on one of these so-called universal vaccine targets," Lingwood says. "When there's a refocusing event, that means we can swing the antibody response against that target, which under other conditions is simply not seen. We have shown in previous studies that when you're able to elicit this kind of response, it's protective against flu strains that mimic pandemic threats."
Influenza Virus (Flu)
Nearly everyone has experienced the fever, aches, and other symptoms of seasonal flu that afflicts 5 – 20 percent of Americans each year. Although these yearly flu epidemics can be fatal in some people, such as the elderly, young children, and people with certain underlying heath conditions, flu is generally not a life-threatening disease in healthy individuals.
Flu, or influenza, is a contagious respiratory illness that spreads from person to person through the air via coughs or sneezes or through contact with infected surfaces. It is caused by a group of continuously changing viruses called influenza viruses.
Influenza viruses change easily and often, they are unpredictable, and they can be deadly. It is always a great concern when a new flu virus emerges, because the general population does not have immunity and almost everyone is susceptible to infection and disease.
Every few decades or so, a new version of the influenza virus emerges in the human population that causes a serious global outbreak of disease called a pandemic. Pandemics are associated with widespread illness - and sometimes death - even in otherwise healthy people. These outbreaks can also lead to social disruption and economic loss.
About a decade ago, scientists and public health officials feared that we might be on the brink of a pandemic caused by the so-called avian or bird H5N1 flu that began circulating among poultry, ducks, and geese in Asia and spread to Europe and Africa. To date, the avian flu virus has not acquired to ability to spread easily from person to person – a necessary step in order for a virus to cause a pandemic.
In the spring of 2009, a different influenza virus - one that had never been seen before - suddenly appeared. The novel virus, commonly called swine flu, is named influenza A (H1N1). Unlike the avian H5N1 flu, the H1N1 swine flu is capable of being transmitted easily from person to person. Fortunately, however, H1N1 is far less deadly than the H5N1 virus. In only a few short weeks after emerging in North America, the new H1N1 virus reached around the world. As a result of the rapid, global spread of H1N1, the first pandemic of the 21st century was declared in June of 2009.
Although the 2009 H1N1 pandemic did not turn out to be as deadly as initially feared, the next pandemic flu virus could emerge at any time, and we must remain vigilant. Hopefully, the knowledge gained in response to the H5N1 and 2009 H1N1 outbreaks, and continued research to more completely understand influenza virus, as well as improvements in vaccine and drug development, will enable us to minimize the effects of future influenza outbreaks.
Different Types of Influenza Virus
There are three different types of influenza virus – A, B, and C. Type A viruses infect humans and several types of animals, including birds, pigs, and horses. Type B influenza is normally found only in humans, and type C is mostly found in humans, but has also been found in pigs and dogs.
Influenza pandemics are caused by type A viruses, and therefore these are the most feared type of influenza virus neither types B or C have caused pandemics.
Type A influenza is classified into subtypes depending on which versions of two different proteins are present on the surface of the virus. These proteins are called hemagglutinin (HA) and neuraminidase (NA). There are 17 different versions of HA and 10 different versions of NA. So, for example, a virus with version 1 of the HA protein and version 2 of the NA protein would be called influenza A subtype H1N2 (A H1N2, for short).
The influenza A subtypes are further classified into strains, and the names of the virus strains include the place where the strain was first found and the year of discovery. Therefore, an H1N1 strain isolated in California in 2009 is referred to as A/California/07/2009 (H1N1).
Although many different combinations of the HA and NA proteins are possible, viruses with only a few of the possible combinations circulate through the human population at any given time. Currently, subtypes H1N1 and H3N2 are in general circulation in people. Other combinations circulate in animals, such as the H5N1 virus found in birds. The subtypes that exist within a population change over time. For example, the H2N2 subtype, which infected people between 1957 and 1968, is no longer found in humans.
What Influenza Viruses Are Made of
Influenza virus has a rounded shape (although it can be elongated or irregularly shaped) and has a layer of spikes on the outside.
There are two different kinds of spikes, each made of a different protein – one is the hemagglutinin (HA) protein and the other is the neuraminidase (NA) protein.
The HA protein allows the virus to stick to a cell, so that it can enter into a host cell and start the infection process (all viruses need to enter cells in order to make more copies of themselves).
The NA protein is needed for the virus to exit the host cell, so that the new viruses that were made inside the host cell can go on to infect more cells. Because these proteins are present on the surface of the virus, they are “visible” to the human immune system.
Inside the layer of spikes, there are eight pieces, or segments, of RNA that contain the genetic information for making new copies of the virus. Each of these segments contains the instructions to make one or more proteins of the virus. So for example, segment 4 contains the instructions to make the HA protein, and segment 6 contains the instructions to make the NA protein (the segments are numbered in size order, with 1 being the largest).
When new viruses are made inside the host cell, all eight segments need to be assembled into a new virus particle, so that each virus has the complete set of instructions for making a new virus. The danger occurs when there are two different subtypes of influenza A inside the same cell, and the segments become mixed to create a new virus.
How Influenza Viruses Change
Influenza virus is one of the most changeable viruses known. There are two ways that influenza virus changes – these are called drift and shift.
Drifting, or antigenic drift, is a gradual, continuous change that occurs when the virus makes small “mistakes” when copying its genetic information. This can result in a slight difference in the HA or NA proteins. Although the changes may be small, they may be significant enough so that the human immune system will no longer recognize and defend against the altered proteins. This is why you can repeatedly get the flu and why flu vaccines must be administered each year to combat the current circulating strains of the virus.
Shifting, or antigenic shift, is an abrupt, major change in the virus, which produces a new combination of the HA and NA proteins. These new influenza virus subtypes have not been seen in humans (or at least not for a very long time), and because they are so different from existing influenza viruses, people have very little protection against them. When this happens, and the newly created subtype can be transmitted easily from one person to another, a pandemic could occur.
Virus shift can take place when a person or animal is infected with two different subtypes of influenza. Take the case, for example, where there are two different subtypes of influenza circulating at the same time, one in humans and one in ducks. The human subtype is able to infect humans and pigs, but not ducks, while the duck subtype is able to infect ducks and pigs, but not humans. When a pig becomes infected with both the human and duck influenza subtypes at the same time, the segments of both viruses are scrambled or reassorted. inside an infected pig cell. As a result, a human virus particle could assemble that contains the duck HA segment instead of the human HA segment. A new virus subtype has been created. This new subtype could infect humans, but because it has the new duck version of the HA protein, the human immune system would not be able to defend an infected person against the new virus subtype. The virus could continue to change to allow it to spread more easily in its new host, and widespread illness and death could result.
Virus shift can also occur when an avian strain becomes adapted to humans, so that the avian virus is easily transmitted from person to person. In this case, the avian strain jumps directly from birds to humans, without mixing or reassortment of the genetic material of influenza strains from different species.
Influenza Epidemics and Pandemics
Influenza epidemics, also known as seasonal flu, occur annually and are the most common emerging infection among humans. These epidemics have major medical impacts, but they are generally not fatal except in certain groups such as the elderly.
Pandemics, on the other hand, happen once every few decades on average. They occur when a new subtype of influenza A arises that has either never circulated in the human population or has not circulated for a very long time (so that most people do not have immunity against the virus). The new subtype often causes serious illness and death, even among healthy individuals, and can spread easily through the human population.
There were three influenza pandemics in the 20th century – the “Spanish” flu of 1918-19, the “Asian” flu of 1957-58, and the “Hong Kong” flu of 1968-69. The 1918 flu, caused by a strain of H1N1, was by far the most deadly. More than 500,000 people died in the United States as a result of the Spanish flu, and up to 50 million people may have died worldwide. Nearly half of those of those deaths were among young, otherwise healthy individuals. The 1957 pandemic was due to a new H2N2 strain of influenza virus that caused the deaths of two million people, while the 1968 pandemic resulted from an H3N2 strain that killed one million people.
One pandemic has occurred so far in the 21st century. This was due to the novel swine-origin H1N1 virus which emerged in 2009.
The WHO established a six phase pandemic alert system in 2005 in response to the potential threat of the H5N1 avian influenza virus. The alert system is based on the geographic spread of the virus, not necessarily the severity of disease caused by the virus. Although a disease may be “moderate” in severity, during widespread outbreaks, declaration of a pandemic is beneficial because it accelerates the vaccine production and prompts governments to take extra measures to contain the virus. Travel and trade bans may be implemented in some cases, although if the disease is already widespread, these may not be considered effective.
Prior to the emergence of the 2009 H1N1 virus, the alert level stood at Phase 3 based on the circulation of the H5N1 virus. On April 27, 2009, after the H1N1 flu virus was recognized to be passing from person to person in Mexico, the alert level was raised to Phase 4. Two days later, on April 29, the WHO again increased the alert level, this time to Phase 5, reflecting the sustained transmission of the novel H1N1 virus in the United States. As H1N1 continued to spread worldwide and infect people in over 70 countries, the WHO raised the alert to Phase 6 – the highest level - on June 11, 2009. Over the next few months, H1N1 spread to more than 200 countries and territories worldwide. The Phase 6 alert of the 2009 H1N1 pandemic was declared by the WHO to have ended on Aug. 10, 2010.
Influenza naturally infects wild birds all around the world, although they usually do not become ill. The virus is very contagious, however, and it can become a problem when the virus is transmitted to domesticated birds, such as chickens, ducks, or turkeys, because domesticated poultry can succumb to illness and death from influenza.
Humans generally do not become infected with avian flu. That is why news of humans contracting avian influenza during an outbreak of bird flu in poultry in 1997 in Hong Kong was alarming. It indicated that the virus had changed to allow it to directly infect humans. The virus that caused this particular outbreak is influenza A subtype H5N1.
Since 1997, H5N1 infections in birds have spread, initially throughout Asia. Then as birds traveled along their migratory routes, H5N1 dispersed to Russia and Europe, and later to countries in the Middle East and on the African continent.
Most human cases of H5N1 influenza have been traced to direct contact with infected poultry, but there have been a few cases of person-to-person transmission, particularly in clusters where multiple family members became infected.
One reason why avian H5N1 is not readily transmissible among people has to do with the hemagglutinin, or HA, protein of the virus that determines which cell type the virus can enter. As with other viruses, the influenza virus must attach to specific proteins called receptors on the outside of cells in order to gain entry into cells and cause an infection. Unlike human influenza viruses, which infect cells high in the respiratory tract, the H5N1 HA protein attaches to cells much lower in the respiratory track. The virus is so deep within the respiratory tract that it is not coughed up or sneezed out, and so it does not easily infect other people. If the HA protein of H5N1 were to mutate so that it could infect cells higher in the respiratory tract, then it would more likely be able to pass from person to person.
As of July 2015, there have been some 840 laboratory-confirmed cases of H5N1 infections in humans, in 16 different countries, and close to 450 deaths. The countries with the overall highest case numbers are Egypt, where almost all cases in 2015 have occurred, followed by Indonesia and Vietnam.
H5N1 continues to circulate in poultry, and small and sporadic clusters of human infections are still occurring. However, H5N1 currently does not transmit easily between people, so the risk of a large outbreak is low at this time.
Highly pathogenic H5 avian virus infections were first reported in birds in the United States in December 2014. Over approximately the next six months, more than 200 findings of infection with H5N2, H5N8, and H5N1 viruses were confirmed, mostly in poultry including backyard and commercial flocks. More than 40 million birds in 20 states were either infected or exposed. No human infections by these H5 viruses have been reported in the United States, but their presence in birds makes it more likely than human H5 infections could occur in the United States. Individuals having close contact with live infected poultry or surfaces contaminated with the avian influenza viruses are at highest risk of infection in places where the viruses circulate. There have been no reports of infection occurring from eating properly cooked poultry.
In addition to the H5 viral subtypes, other avian influenza strains have occasionally infected humans in recent years. These include the H7N2 strain which infected two individuals in the eastern United States in 2002 and 2003, and the H9N2 strain which has caused illness in several people in Asia in 1999 and 2003.
In March of 2013, a new subtype of avian influenza was found to infect humans. Influenza A (H7N9) had previously been detected in birds, but this particular variant had never been seen before in humans or animals. The initial wave of H7N9 infections occurred in the spring of 2013 in China, followed by a larger, second wave in the first half of 2014 in China and a few neighboring countries. As of February 2015, approximately 570 cases and 210 deaths have been reported to the WHO, mostly in China. People in the majority of cases had exposure to infected poultry or contaminated environments. The H7N9 virus causes a severe respiratory illness in most infected people, but it currently does not appear to spread easily from person to person.
Swine influenza, or swine flu, is a very contagious respiratory disease of pigs. Although pigs become ill, they generally do not die from swine flu viruses.
In April of 2009, an influenza virus originating in swine was discovered to be capable of infecting humans and spreading from person to person. The new virus is named influenza A (H1N1), although it is commonly referred to as swine flu. Although it is called swine flu, the new H1N1 virus is transmitted from person to person, and not through contact with pigs or pork products.
The new H1N1 virus is made up of a novel combination of segments from four different influenza virus strains - a Eurasian swine virus, a North American swine virus, and avian and human influenza virus segments. Reassortment of segments from these different viruses produced a unique virus that had not been seen before by the human population. When novel viruses like this emerge, natural immunity is usually limited or nonexistent in humans.
The H1N1 influenza virus outbreak originated in Mexico in early 2009, and then spread rapidly throughout North America. Within a few weeks, the novel swine-origin H1N1 virus extended its reach around the globe. In June 2009, as a result of the global spread of the H1N1 virus, the WHO issued its first pandemic declaration of the 21st century - the first since the flu pandemic of 1968. The pandemic declaration acknowledged the inability to contain the virus and recognized its inevitable further spread within affected countries and into new countries. The new H1N1 virus became the dominant influenza strain in most parts of the world, including the United States.
Like other influenza pandemics, the 2009 H1N1 outbreak occurred in waves. The first wave took place in the spring of 2009, with a second wave commencing in late August as children and college students returned to classes. The outbreak peaked in October of 2009, with flu activity reported in all 50 states, as well as numerous other countries and territories. By January 2010, flu activity had returned to below baseline levels.
The H1N1 virus continues to circulate at low levels, but it is no longer the dominant influenza strain, and its behavior more closely resembles a seasonal influenza virus than a pandemic flu.
From the time the outbreak began in April 2009 through April 2010, the CDC estimated that about 60 million Americans became infected with the H1N1 virus, 265,000 Americans were hospitalized and 12,000 deaths occurred as a consequence of the 2009 H1N1 flu. The highest hospitalization rates occurred in young children. Exact numbers are not known due to the widespread nature of the outbreak and because most patients, especially those with mild cases, were not tested. The large majority of infections in the United States and most other countries were mild, although pregnant women and individuals with certain underlying medical conditions had an increased risk of severe and fatal illness.
There were some differences between the pandemic H1N1 flu and regular, seasonal flu. First, the H1N1 flu continued to spread during the summer months, which is uncommon for seasonal flu. Second, a much larger percentage of H1N1 patients exhibited symptoms of vomiting and diarrhea than is common with regular seasonal flu. There were also more reports of severe respiratory disease, especially in young and otherwise healthy people, infected with the new H1N1 virus than with seasonal flu viruses.
Significantly, the majority of cases of H1N1 infection, including severe and fatal cases, occurred in young and otherwise healthy individuals generally between the ages of 5 and 50, with relatively few deaths among the elderly. This is in contrast to the situation with seasonal flu which primarily afflicts the very young and the elderly, and where 90 percent of severe and lethal cases occur in people over the age of 65. Deaths among the elderly accounted for only 11 percent of H1N1 deaths.
Fortunately, the 2009 H1N1 flu was sensitive to two antiviral drugs used to treat influenza - Tamiflu® (oseltamivir) and Relenza® (zanamivir). The drugs act by inhibiting the essential neuraminidase protein (the “N” protein in the naming system). Proper use of these drugs can shorten the duration and lessen the severity of the sickness and reduce the chance of spreading the disease. The drugs reduce the risk of pneumonia - a major cause of death from influenza - and the need for hospitalization. To be most effective, the antiviral drugs should be administered as soon as possible after the onset of symptoms.
A vaccine to protect against the H1N1 virus was developed, tested, and approved and became available in October 2009. Due to the fact that the virus used to prepare the vaccine grew more slowly than most seasonal flu viruses do, production of the vaccine lagged and widespread distribution of the vaccine occurred later than anticipated. Priority for the vaccine was initially given to health care and emergency workers and individuals at high risk for severe disease, but by the winter of 2009-2010 availability was extended to the general population. Later, some doses went unused.
Although some had concerns about the safety of the H1N1 vaccine, flu vaccines have a very good safety profile. While mild side effects, such as soreness at the site of injection, aches, and low-grade fever, may occur as a result of receiving a flu shot, it is not possible to get the flu (H1N1 or seasonal) from the vaccine. The flu shot, or inactivated vaccine, is made from only a portion of the virus – a purified protein that makes our immune system develop protection. Likewise, the nasal spray version of the flu vaccine contains attenuated or weakened virus that is not able to cause the flu. Given the potential serious health outcomes from the flu, especially for high-risk population groups, the benefits of vaccination as the best way to prevent influenza infection and its complications far outweigh the risk of relatively minor side effects from the vaccination.
Injecting something into your body can be concerning for some, especially when you're unsure of what's inside the needle. We're here to take the mystery out of a vaccine's ingredients.
A vaccine contains a part of a germ (bacteria or virus) that is called an antigen. The antigen has already been killed or disabled before it's used to make the vaccine, so it can't make you sick. Antigens are substances, often a protein, that stimulate the body to produce an immune response to protect itself against attacks from future actual disease exposure. In addition, vaccines contain other ingredients that make them safer and more effective, including preservatives, adjuvants, additives and residuals of the vaccine production process. Because specific ingredients are necessary to make a vaccine, even though they are eventually removed, trace amounts can still remain. These residuals can include small amounts of antibiotics and egg or yeast protein. The American Academy of Pediatrics also provides a good explanation about what's inside the vaccine needle.
If you're a parent concerned that your child may be exposed to too many antigens, there's no need to worry: Today's vaccines contain far less antigens than in the past, thanks to advances in biomedical science. Additionally, children's bodies are well equipped to handle many antigens at the same time. A healthy baby can accommodate multiple vaccinations because vaccines, and the antigens they contain are designed for babies' immune systems. In fact, babies can handle significantly more antigens than those that are found in vaccines.
A few years ago, much attention was placed on thimerosal, an organic form of mercury (also called ethylmercury) that prevents vaccines from being contaminated. This form of mercury is different from methylmercury, which can damage the nervous system. Although thimerosal has been shown to be safe, now all routine childhood vaccines are produced in thimerosal-free form. This includes the flu vaccine.
There is an urgent need to utilize novel platforms that can lead to the development of more effective vaccines and therapeutics for influenza, which continues to cause a significant burden of disease. Human challenge models have been successfully used for centuries. With advancing technologies and new methods to investigate the host-pathogen interaction, human challenge studies will be essential for progress, and can be performed in a safe and ethical manner. Furthermore, systems biology (e.g., transcriptomics, metabolomics, proteomics, lipidomics, etc.) allows for fundamental changes and patterns of the human immune system to be dissected. Harmonizing these two modalities is very promising future studies should address using systems biology in a human challenge model to identify important gaps in our knowledge of influenza pathogenesis, and identify essential pathways involved in producing effective immune responses to vaccination. The ultimate goal would be to use these methods in concert to discover novel therapeutics, and potentially even lead to the development of a universal influenza vaccine.
A Primer for the Media on Viruses, Vaccines, and Covid-19
2020 is a year when many things besides people have died, or at least placed on indefinite life support. Music and most arts and culture (at least audience-based), education, a person`s livelihood, social trust and interaction, common sense and common decency, debate, and we can include responsible journalism to the list.
In fact, responsible journalism was one of the first casualties of 2020 and bears responsibility for much of the rest.
My path to 2020 was unusual, to say the least, but it prepared me to deal with the events that have transpired. Each step of my career as a scientist I chose a path which led me to 2020. Here are some examples:
- My two leading choices for the Ph.D. program in chemistry were at the University of Southern California (USC), where I had interviewed with Professor George A. Olah (Nobel Prize in Chemistry, 1992), and the University of California, Riverside (UCR). I chose UCR and Professor M. Mark Midland, who had earned his degree with Professor Herbert C. Brown (Nobel Prize in Chemistry, 1979) and was young, enthusiastic, and broad-based in his interests . If I had chosen and been able to study with Dr. Olah, my career would have been set but much more narrowly focused. I chose Dr. Midland and I have never regretted the choice.
- With the Ph.D. in hand, I had a choice of academia (the expected route) or industry. I chose industry, specifically, the pharmaceutical industry since I had always been interested in medicinal applications and medicine in general.
- In industry, I chose development over research based upon the unique challenges.
- Later, I chose to move out of direct scientific work and into Quality Assurance. Part of this choice was the opportunity to learn new things.
- Still later, I chose to move into Biopharmaceuticals and vaccines in particular. This afforded me a new opportunity at learning.
- Finally, I moved into consulting to try and use my experience to assist others in the industry.
The last company I worked for was a vaccine company, as Director of QA. For those that do not understand, being responsible for Quality Assurance is an immense task. You have to be both an expert and a judge.
The company was founded in an attempt at development of an HIV vaccine. After 9/11, the company expanded into Biodefense and was pursuing the development of vaccines for anthrax and smallpox for the US National Stockpile as part of the newly formed Dept. of Homeland Security. I joined the company at that time and I became the project leader on a new smallpox vaccine being developed in collaboration with a Japanese company.
I had studied virology and infectious diseases in college, but I needed to expand my knowledge. So, it was immersion time. This also coincided with the original SARS outbreak in Hong Kong. In fact, I visited Hong Kong in 2003 during SARS (no lockdowns, distancing, etc. some people wore masks but it was mainly because of the very poor air quality in Hong Kong, not due to SARS). I had become interested in Upper Respiratory Infections (URI) long before, mainly as a result of my occasional personal battles with the cold, flu, sinusitis, bronchitis, etc. but SARS was a new opportunity.
As a project leader for smallpox, I had the opportunity to meet and talk with Dr. D.A. Henderson, a leading person during the WHO smallpox eradication effort during the 1960s and 1970s and involved with the Dept. of Homeland Security on the Biodefense initiative under the G.W. Bush administration.
An hour or two with Dr. Henderson was worth a whole semester of classroom learning. I learned much about infectious disease control, strategy, management, etc. Of course, Dr. Henderson would be opposed, to put it mildly, to the current “policies” being used, such as lockdowns, closures, masking, etc.
However, at the time that I met him, much of the concern was directed towards the aging U.S. vaccine stockpile, particularly for infectious diseases that were being considered as possible bioterrorism weapons (e.g. anthrax and smallpox).
After “retiring”, I had hoped that I was “riding off into the sunset” on a Harley (figuratively, since I do not yet own one) as far as my career was concerned. But,as a scientist, with expertise in infectious diseases, PPE, antiviral medicines, vaccines, etc., this year thrust me back into thinking mode, instinctively at first. But, I soon discovered that we were in trouble, not from the virus but from ourselves.
As if a switch had been thrown, the light went out on responsible journalism EVERYWHERE! Power has not yet been restored.
I came upon an article recently on Yahoo from Zacks that caught my attention . The opening sentence really got me going and I quote it now (emphasis added):
Biotech firms and drugmakers across the globe are pumping in millions of dollars to develop a vaccine to wipe out the deadly coronavirus, with many already ramping up production of their vaccine candidates if one gets an approval.
With this one sentence and a simple phrase in it, the hammer was hit right on the head of irresponsible and misinformed journalism. Normal journalism would have written simply “…a vaccine for coronavirus…” but hyperbole won out.
There are two aspects to that phrase that are worth examining, i.e. the idea of a vaccine wiping out a virus and the concept of a deadly virus. I have heard the term “wiping out” before (Nancy Pelosi?). But, I want to first deal with the deadly virus hyperbole and get to the vaccine part later.
How “deadly” is coronavirus? NOT VERY and that is based on data, medical reports, and general knowledge of URI.
It is interesting to review the first confirmed case in the US. Fortunately, this case history has been published. This person, a male in his 30s, had returned from Wuhan in mid-January after visiting family and had developed a cough and nausea. He was in a suburb north of Seattle, Washington.
As it so happened, I was visiting that area at the same time. He happened to have seen a CDC alert about Wuhan and went to a clinic. At the time, his main symptoms were cough and nausea and only intermittent low fever. His initial examination presented with no fever and his chest x-ray and lab tests were all normal. Even the clinicians recognized the implications as evidenced by the following statement from the case study:
These nonspecific signs and symptoms of mild illness early in the clinical course of 2019-nCoV infection may be indistinguishable clinically from many other common infectious diseases, particularly during the winter respiratory virus season.
He was admitted into isolation as he was being tested for the new strain of coronavirus (there have been 4 known strains prior to this: HKU1, NL63, 229E, and OC43). Once confirmed as having the new strain, he received only supportive care. It should be noted that besides nasal swabs containing virus, his feces also tested positive (which was tested since he was experiencing some gastrointestinal symptoms).
After several days, he developed pneumonia, which the staff feared was hospital-acquired pneumonia. This pneumonia is a serious problem because they tend to be antibiotic resistant strains. As a result, he was started on vancomycin (the only effective antibiotic against resistant strains) and also was given remdesivir. He recovered quickly and eventually was released.
The source of his infection was never traceable since he reported no contact with ill people while in Wuhan. It is not known if he picked up the virus while in Wuhan, or in transit, or even after returning to the US. At the end of the case study report, January 30, no secondary transmissions had been identified as known contacts had not yet become sick. This case does not mirror the panic that has been imposed concerning this disease.
After reading this, I have considered what would have happened had this person NOT reported to a clinic. It is hard to say. Eventually, there would have been a first confirmed case, but when and where? How many cases would have gone unnoticed in the meantime? Would this person’s disease have faded without experiencing pneumonia? He responded quickly to medical intervention, which was mainly to fight a BACTERIAL infection (pneumonia) that was possibly acquired in the hospital setting. He did quite well against the virus.
The media hype over this case at the time focused heavily on his Wuhan trip. How many people experienced the same symptoms and dismissed them because they had no Wuhan connection?
But, soon the media was all about the most serious symptoms, high fever, serious fatigue, difficulty breathing. If one went to the medical sites, as I did, you would find the same general advice, i.e. treat it like you would the flu but if it starts becoming worse, call or go see a doctor.
So, most people were probably paying attention to the media reports and not recognizing the actual medical reports. How many people were experiencing the mild form and dismissed it because it did not fit the serious symptoms reported by the media?
To this day, little has changed. The vast majority of people experience mild symptoms. Higher risk individuals sometimes experienced the more serious symptoms. Symptoms vary depending on the individual, their immune system, viral load, etc.
Meanwhile, around the world, more cases were becoming known as was the relatively benign nature of the virus by most people who experienced it. It was known early on in China that the high risk group for serious disease was the same as influenza that is, elderly with serious health problems, but this was not being communicated. Even so, we had plenty of other data as well.
In February, the virus was discovered on a cruise ship in Japan. A ship mostly carrying retired, elderly people. It was an opportune situation to observe this virus. About half of the people on the ship tested positive (672 positive) and remained quarantined on the ship. There were a few deaths (13 in total), but most people experienced mild disease and eventually were released from the ship or hospital. Some Americans were returned to the US despite the travel bans. Still, it was clear that the virus was not deadly and it was clear who was at risk.
We all know what happened in March. The virus did not change nor did the data, bad modeling was pushed and governments panicked. There is little need to go into detail about the time since March.
So, now that several months have elapsed, what do we know about the mortality? First, it is becoming clearer that the mortality rate of Covid is consistent with influenza. There is nothing so different about it. This is based on serology studies to try and define a baseline number of people who have experienced the virus, not on testing since the testing numbers have little value. Far more people have experienced the disease than the numbers indicate. But the mortality is not so much due to the virus, but rather the susceptible population.
The national average on mortality rate, all causes, is running about 110-111% of expected. This number has actually risen over the last month or two even though the Covid death rate has declined. The top 5 highest values are for NYC (176%, note: the CDC reports NY state separately), New Jersey (134%), Arizona (124%), NY State (121%) and D.C (129%). There are seven states/territories that are below the 100% level (Puerto Rico, West Virginia, North Dakota, North Carolina, Montana, Hawaii, and Alaska). The Non-lockdown states are Arkansas (108%), Iowa (105%), Nebraska (102%), North Dakota (99%), South Dakota (100%), Utah (108%), and Wyoming (107%). A few other states worth noting are California (110%), Michigan (113%), Massachusetts (117%), Florida (114%), and Texas (115%).
What do these numbers mean? The CDC calculates expected mortality. They do this looking at the populations, age of population, health characteristics, recent historical trends, averages across various diseases and conditions, etc. Yes, it is computer modeling. People might expect that given the hype on Covid the mortality rates should be high. Well, let’s see.
The current number of reported deaths related to Covid is about 180,000, although that number is maybe meaningless because there is no consistency in reporting and we do not know how deaths are being recorded. Just because a person dies and maybe they have the virus does NOT mean that the virus or even a complication was the cause of death. Nationally, we know that deaths related to Covid have been accounting for about 5-6% of overall mortality and while that number was slightly higher earlier during lockdowns, it has been drifting downwards for some time. But, those deaths are probably not contributing significantly to the excess mortality figures.
Why? Because, the vast majority of deaths are in the elderly, age 70+, with serious health issues. These people have already been mostly calculated into 2020 mortality. In other words, they are at high risk of death from many things, not just coronavirus. They would experience the same outcome if it were influenza, maybe even rhinovirus. Certainly, bacterial infections would cause the outcome (and in the majority it has been pneumonia causing death, not Covid). Their life expectancy before coronavirus was already short – they were probably not expected to make it into 2021. That has been calculated into the expected mortality. Remember, the life expectancy in the US is about 78 years.
I know some people cringe when this kind of analysis is done. But, like a medical examiner doing an autopsy, in order to adequately understand what you are doing, you need to put aside the emotional aspects and focus on learning what you can learn. I especially feel for the elderly in care facilities and the poor in the inner cities who had this virus thrust upon them by horrible policies. They had no choice. Hopefully, by being honest with analysis, we can avoid the same mistakes in the future.
In fact it was the latter segment of society that may have an impact on the mortality number since the poorer communities were the ones to have been hit hard by the lockdown orders and virus. Minorities between the ages of 50-65 tend to have a higher death rate than would be normal course. Certainly, it is higher than their, shall we say, suburban counterparts.
So, where do mortality increases actually come from? The news media is paying little attention to this question. One source is collateral damage from another war started by our government decades ago. The “War on Drugs” was started in the 1980s. The following chart shows deaths by overdose (OD) in the US since that time. In 2019, 71,000 people died from OD in the US.
Recently, the American Medical Association (AMA) issued an emergency alert for an alarming increase observed in OD deaths in over 40 states in 2020. They predicted 2020 was going to be worse than 2019! They consider it a state of National Emergency.
While the data is hard to find at this point, there are reports that suicides are also increasing in 2020. This should not be surprising given the huge emotional and mental strains imposed on people during 2020 by their governments.
OD and suicide deaths tend to be mostly in younger, healthier people under the age of 50 who ARE NOT calculated significantly into the mortality rate. OD and suicides are calculated into the expected mortality but based upon past history so if there are sudden surges upward, it will reflect in the overall mortality.
Other diseases are also contributing simply because of the restrictions placed on receiving medical care during the pandemic, something which violates the Hippocratic Oath. Pneumonia deaths with no connection to either influenza or coronavirus are more prevalent than pneumonia deaths related to either viral infection.
So, is coronavirus deadly? Not really in fact, most viruses are not truly deadly. The outcome may be death, but that is different than actually being deadly. A bite from a black mamba snake is deadly due to the potent venom. Viruses are parasites, unlike bacteria. Viruses depend on the support of their host. If a virus is to survive, it needs the host to survive. What kills most people with viruses is their own immune system weakness, but sometimes the immune overreaction can kill. That weakness is taken advantage of by bacterial infections. Also, generally poor health conditions can lead to organ failure.
During this pandemic, the vast majority of deaths have occurred in elderly people with serious health issues. These people would experience the same result if they had acquired influenza. As a matter of fact, it is quite likely that they would have the same result if the virus was rhinovirus. They would likely have the same result if they had bronchitis, sinusitis, pancreatitis, gastritis, bladder infection, etc. Their system simply was not able to fight the disease. Period.
To the vast majority of people who have experienced this disease, it is not even close to “deadly.”
“A Vaccine to wipe out the deadly coronavirus”
Well, the coronavirus is not deadly. But, what about the “vaccine” part of the statement?
No vaccine “wipes” out a virus. Vaccines are not cures. Vaccines are not preventatives. Vaccines do not seek out and destroy. As an example, we have had vaccines for influenza for decades (since the 1940s) and each year influenza exacts a toll on humans, including sometimes those who have been vaccinated. Influenza is not even close to being “wiped out.” We manage it at best.
Here is a short list of infectious diseases that are a part of our natural existence and any of these have the potential to cause death in any given individual..
1. Bacterial Infections. (Cocci) Pneumonia, Staphylococcal, Streptococcal, Enterococcal, Toxic Shock (Gram Positive Bacilli) Diphtheria, Anthrax, Listeriosis (Gram Negative Bacilli) Cholera, Trench Fever, E. Coli, Plague, Salmonella
2. Spirochetes Infections. Lyme disease, Yaws, Leptospirosis
3. Anaerobic Bacterial Infections. Botulism, Tetanus, Clostridium
4. Rickettsiae Infections. Murine Typhus, Rocky Mountain Spotted Fever
5. Mycobacteria. Tuberculosis, Leprosy
6. Fungal Diseases. Aspergillosis, Candidiasis, Histoplasmosis
7. Parasitic Infections. Nematodes (roundworms), Trematodes (flukes), Cestodes (tapeworms)
8. Protozoan Infections. Amebiasis, Giardiasis, Malaria, Encephalitis, Toxoplasmosis
9. Respiratory Viruses. Influenza/Parainfluenza, Adenovirus, Rhinovirus, Coronavirus
10. Herpes Viruses. Chickenpox, Mononucleosis, Cytomegalovirus, Herpes Zoster
11. Enteroviruses. Polio, Hand-Foot-Mouth Disease (not the same as the politician’s “foot-in-mouth” disease)
12. Various Viradae Viruses. Dengue, Hanta, Lassa, Ebola, Marburg, Yellow Fever
13. Immunodeficiency Virus. HIV
14. Misc. Viruses. Measles, Mumps, Rubella, Smallpox
15. Sexually Transmitted Diseases. Syphilis, Gonorrhea
Many of these diseases have vaccines available, many do not. Some vaccines are more effective than others. But there has been only one that we have eradicated naturally, i.e. “wiped out,” and that is smallpox.
Smallpox has been known as long as human existence. There is evidence from archeological studies that ancient Egyptians suffered from smallpox based upon descriptions and artistry. Many historically famous people experienced smallpox and survived (Mozart and Lincoln are two notable examples). Finally, in the mid-20 th century, it took a worldwide effort lasting over a decade to do it. Here are some of the main reasons why it was possible:
1. Smallpox was entirely a human disease. It did not “toggle” back and forth between other mammalian species.
2. The symptoms of smallpox were unique and quite recognizable. This meant that it was easy to identify a person who was sick with smallpox and quarantine them. It was just as easy to identify contacts and observe them.
3. The vaccine was quite effective. As far as vaccines go, it was very effective, probably because of #1 above. However, the vaccine also had serious side effects. A small percentage of people experienced these very bad effects, sometimes fatal. In fact, one of the reasons for the new initiative after 9/11 was the concern over the safety of the old vaccine. During the eradication effort, the safety profile was accepted against the goal of eradication. But, in today’s world, the serious side effect potential was considered too great. We could now do better.
4. A massive effort was undertaken to go to every place on Earth to try and eliminate the disease. This effort was started several years before the WHO eradication effort. The vaccine had been used in most non-third world countries and there was little incidence of the disease. Usually, the disease was brought back by an aid worker going into some part of a third world country where the virus was still prevalent.
What exactly does a vaccine do?
Under the best of circumstances, a vaccine acts as a primer to the immune system. That is, it “inspires” the immune system to respond as if a true infection has occurred, albeit at a reduced scale. That is, to produce antibodies specific to the virus or surrogate used in the vaccine (antigen). The idea is that if a person is exposed to the real virus (true antigen) at a later time, the immune system will recognize it and respond quicker and more efficiently than normal. This may allow the immune system to gain control of the viral load before it can go to a threshold where disease symptoms are exhibited.
The vaccine usually is some weakened form of the original virus, maybe even inactivated, or it may be a chemical or structural surrogate, i.e. similar in composition but not active.
It is not a preventative! The vaccine does not somehow block the entry of the virus into your body. The vaccine only acts to initiate maybe a quicker more efficient immune response once infection has occurred.
It does not wipe out the virus! In fact, it does nothing to directly interact with a virus either in or out of the body.
The vaccine does not actually do any damage to the virus in your body it is not a therapy or “antiviral” medicine. If your body has produced antibodies that are effective, they will seek out the virus. The antibodies are your weapon. The vaccine does not play any direct role against the virus.
The vaccine does nothing to the virus molecule that exists outside of your body. You could spray vaccine everywhere in the environment and it would have ZERO effect. Disinfecting agents like bleach, UV radiation, low or high pH solutions, etc. will break the virus molecule down but not the vaccine.
After decades of vaccines for influenza, we have not been able to eradicate influenza, why? It goes to the reasons why we were able to eradicate smallpox. First, URI such as influenza and coronavirus are carried by other mammalian species besides humans. Birds, pigs, and even domestic cats can carry the virus. So, in order to eradicate the virus, we would have to start by eradicating all of the birds, pigs, and cats in the world, maybe all mammals because we maybe do not yet know all of the species that may be capable of carrying the virus. Maybe then we could begin to deplete the molecule and eventually eradicate it.
It is this very reason that we tend to have a low effectiveness of URI vaccines. For this, we need to make clear certain definitions. Let’s use influenza as an example (the same applies to coronavirus). When a person receives an influenza vaccination, given in the muscle of the tricep or back of the arm, within some period of time they usually experience swelling, tenderness, pain, maybe some redness, etc. This is usually an indication that the vaccine has elicited some form of immune response, or a “take”. With influenza vaccines, this has been typically around 90%. Sometimes a second injection will give a take, and sometimes it just doesn’t happen.
For people who may remember the smallpox vaccine, the vaccine was given by stabbing a series of small punctures on the skin of your arm. After a period of time, a sort of blister developed followed by a scab. This was a take of the smallpox vaccine. After the scab fell off, you had a dimpled scar. I still have a scar but it has almost faded out. Under certain conditions I can still see it.
When a vaccine is tested for approval, it cannot be actually tested against the virus. That is, medical ethics do not permit exposing a healthy person to a live virus. So, the logical experiment of giving a vaccine to people and then exposing them to the virus is not performed. In old times it was done that way. The original smallpox vaccine, derived from cowpox serum by William Jenner, was first used on a small boy who was intentionally exposed to smallpox. Fortunately for Jenner, the boy lived and did not develop the disease but that was over 200 years ago and the medical ethics then were nonexistent.
In modern times clinical signs are evaluated, such as take, and serological signs, such as antibodies (that are tested for). The presence of all of these is enough to accept the vaccine as “effective.” However, that does NOT mean that it actually will be effective under normal use.
The other consideration is safety. If the vaccine does not cause disease and does not cause serious side effects, it is considered safe. This can be tested on healthy volunteers.
If both of these are met, it will be approved for use.
Vaccine effectiveness can actually only be inferred after an infectious epidemic/pandemic season. It is determined based upon the number of individuals vaccinated, prevalence of disease, etc. It is a complicated evaluation but one which is performed each year by infectious disease agencies such as the CDC and WHO.
To use influenza as an example, while the influenza vaccine generally has a take rate of about 90%, the effectiveness rate can vary widely depending on the flu season and strain(s) for that season. The following table shows data since 2004 on the calculated “effectiveness” of influenza vaccine.
Most of the time, the effectiveness is below 50%. There are many factors which can determine the effective rate but the health of the individual is always the most important. In the elderly, it is recommended that a double dose be administered. But, there is no data that supports that this is actually beneficial.
What Determines Effectiveness?
The answer comes down to individuality. The factors that will determine the outcome of a person with a viral infection are:
1. General Health. The healthier the person and their immune system, the better.
2. Age. Elderly people, even if healthy, will experience weakening immune systems. It is questionable whether the vaccine even gives any boost to their immune system since it is already weakening due to age. To give a double dose when the immune system is not capable of responding to a single dose is maybe futile.
3. Viral Load. This goes to exposure. For any individual, the more virus you are exposed to and infected with initially, the more difficult the fight against the virus. A large initial viral load, even in a healthy person, could mean stronger symptoms. Conversely, elderly people may still be able to deal with a lighter initial viral load, even though they are old and even if they have health problems.
4. Genetics. Genetics plays a central role in health and immune response. Some people are just more disposed to suffer from infections than others. Just like some people are more prone to certain types of cancers.
5. Environment. Those who require hospitalization, while getting more constant care, also are in an environment of increasing danger, especially from acquired antibiotic resistant infections (as seen above with the first confirmed case). The environment can also come into play with viral load. With any person who is battling an infectious disease, trying to minimize other possible sources of infection is very important. It seems contradictory, but hospitals are oftentimes not the optimal place for treatment.
So, it is difficult to really evaluate how effective vaccines truly are with most diseases. However, if a vaccine is proven safe and it may do some good, it should be considered. Perhaps the vaccine can give enough of a boost to an individual’s immune system to prevent reaching a threshold of viral load that is dangerous.
On a personal note, and this is not meant to be an endorsement of vaccines, I choose to get the influenza vaccine each year. I believe that it is not really necessary as I tend to have a good immune system. However, my philosophy on the immune system is that it needs constant exercise to remain healthy, just like the rest of your body and mind. As long as the vaccine is safe, I reason it to be an additional exercise of my immune system. It maybe will have little effect if I encounter influenza, but, maybe the general strength of the immune system is more enhanced, ever so slightly. But, this is my personal choice I cannot impose this choice on others.
Here is the flip side of the coin. This applies to anyone who has experienced disease.
1. People who have developed immunity do not need a vaccine. So, any person who experienced Covid in 2020 does not require a vaccine so soon (they also do not need to wear any face coverings).
2. These same people have demonstrated that their immune system is quite capable of handling the disease. That means for over 99% of the population, this virus is not deadly.
3. Even in the highest risk population, between 75-90% of those infected survived.
If coronavirus is like influenza, your naturally acquired immunity may not last if the virus mutates. We do not know enough yet to know if or when that may occur. The timing also varies from individual to individual. Still, it is important for people to keep a healthy immune system.
If a vaccine is developed and if a person has had this virus, they will have to make the decision for themselves whether a vaccine is appropriate, perhaps with their personal physician.
It is a personal health choice. The Government should not be making that decision.
Take Home Message
1. The coronavirus, SARS-COV-2, is not “deadly.” It can lead to death in very well-identified segments of the population, e.g. the infirmed elderly or poor, but it is very rarely death by the virus. It may be death by bacteria or other causes, yes, but very rarely, if ever, by virus. This is exactly the same as other URI and many other infectious diseases.
2. The mortality that is associated with Covid has little impact on the expected mortality rate since the population that was most at risk also had a very low life expectancy.
3. Increases in mortality in the US are more likely associated with increases in drug OD and suicides, which are collateral damage due to the policies imposed during 2020.
4. Any vaccine that may be developed and approved for coronavirus is at best a boost to the immune system. It will not prevent infection or wipe out the virus. The degree of effectiveness will only be determined over time.
5. People who have experienced Covid or are otherwise healthy do not need a vaccine. But it should be their choice, as it should be for all.
We have gone most of 2020 without responsible journalism, except in a few places that have refused to go the ugly route. Has it been lost forever or can we recover?
The Influenza viruses section of Virology Journal will publish articles on all aspects of influenza virus research, including molecular genetics, molecular biology, biochemistry, biophysics, structural biology, cell biology, immunology, morphology, and pathogenesis. The section will also welcome the case reports of influenza outbreaks in both human and animal populations, and development and evaluation of vaccines and antiviral compounds in humans and animals.
Conserved methionine 165 of matrix protein contributes to the nuclear import and is essential for influenza A virus replication
The influenza matrix protein (M1) layer under the viral membrane plays multiple roles in virus assembly and infection. N-domain and C-domain are connected by a loop region, which consists of conserved RQMV motif.
Authors: Petra Švančarová and Tatiana Betáková
Citation: Virology Journal 2018 15 :187
Published on: 3 December 2018
Analysis of influenza B virus lineages and the HA1 domain of its hemagglutinin gene in Guangzhou, southern China, during 2016
Few studies have analyzed influenza B virus lineages based on hemagglutinin A (HA) gene sequences in southern China. The present study analyzed the HA gene and the lineages of influenza B virus isolates from Guan.
Authors: Feng Ye, Xiao-juan Chen, Wen-da Guan, Si-hua Pan, Zi-feng Yang and Rong-chang Chen
Citation: Virology Journal 2018 15 :175
Published on: 14 November 2018
Histone acetyl transferase TIP60 inhibits the replication of influenza a virus by activation the TBK1-IRF3 pathway
Influenza A virus (IAV) is an important pathogen that poses a severe threat to the health of humans. Nucleoprotein (NP) of IAV plays crucial roles in the viral life cycle by interacting with various cellular f.
Authors: Guoyao Ma, Lin Chen, Jing Luo, Bo Wang, Chengmin Wang, Meng Li, Chengmei Huang, Juan Du, Jiajun Ma, Yungfu Chang and Hongxuan He
Citation: Virology Journal 2018 15 :172
Published on: 8 November 2018
Isolation and characterization of novel reassortant H6N1 avian influenza viruses from chickens in Eastern China
The H6N1 subtype of avian influenza viruses (AIVs) can infect people with an influenza-like illness the H6N1 viruses possess the ability for zoonotic transmission from avians into mammals, and possibly pose a.
Authors: Haibo Wu, Fan Yang, Fumin Liu, Rufeng Lu, Xiuming Peng, Bin Chen, Hangping Yao and Nanping Wu
Citation: Virology Journal 2018 15 :164
Published on: 24 October 2018
Cirsimaritin inhibits influenza A virus replication by downregulating the NF-κB signal transduction pathway
Artemisia scoparia Waldst and Kit is a famous traditional Chinese medicine widely distributed in Xinjiang, China. Flavonoids extracted from it exhibits inhibitory activities against several influenza virus strain.
Authors: Haiyan Yan, Huiqiang Wang, Linlin Ma, Xueping Ma, Jinqiu Yin, Shuo Wu, Hua Huang and Yuhuan Li
Citation: Virology Journal 2018 15 :88
Bat lung epithelial cells show greater host species-specific innate resistance than MDCK cells to human and avian influenza viruses
With the recent discovery of novel H17N10 and H18N11 influenza viral RNA in bats and report on high frequency of avian H9 seroconversion in a species of free ranging bats, an important issue to address is the .
Authors: Tessa Slater, Isabella Eckerle and Kin-Chow Chang
Citation: Virology Journal 2018 15 :68
Published on: 10 April 2018
Effects of the S42 residue of the H1N1 swine influenza virus NS1 protein on interferon responses and virus replication
The influenza A virus non-structural protein 1 (NS1) is a multifunctional protein that plays an important role in virus replication, virulence and inhibition of the host antiviral immune response. In the avian.
Authors: Jinghua Cheng, Chunling Zhang, Jie Tao, Benqiang Li, Ying Shi and Huili Liu
Citation: Virology Journal 2018 15 :57
Published on: 27 March 2018
Major contribution of the RNA-binding domain of NS1 in the pathogenicity and replication potential of an avian H7N1 influenza virus in chickens
Non-structural protein NS1 of influenza A viruses harbours several determinants of pathogenicity and host-range. However it is still unclear to what extent each of its two structured domains (i.e. RNA-binding .
Authors: Sascha Trapp, Denis Soubieux, Alexandra Lidove, Evelyne Esnault, Adrien Lion, Vanaique Guillory, Alan Wacquiez, Emmanuel Kut, Pascale Quéré, Thibaut Larcher, Mireille Ledevin, Virginie Nadan, Christelle Camus-Bouclainville and Daniel Marc
Citation: Virology Journal 2018 15 :55
Published on: 27 March 2018
Towards a universal influenza vaccine: different approaches for one goal
Influenza virus infection is an ongoing health and economic burden causing epidemics with pandemic potential, affecting 5–30% of the global population annually, and is responsible for millions of hospitalizati.
Authors: Giuseppe A. Sautto, Greg A. Kirchenbaum and Ted M. Ross
Citation: Virology Journal 2018 15 :17
Published on: 19 January 2018
Production of highly and broad-range specific monoclonal antibodies against hemagglutinin of H5-subtype avian influenza viruses and their differentiation by mass spectrometry
The highly pathogenic avian influenza viruses of the H5 subtype, such as the H5N1 viral strains or the novel H5N8 and H5N2 reassortants, are of both veterinary and public health concern worldwide. To combat th.
Authors: Violetta Sączyńska, Anna Bierczyńska-Krzysik, Violetta Cecuda-Adamczewska, Piotr Baran, Anna Porębska, Katarzyna Florys, Marcin Zieliński and Grażyna Płucienniczak
Citation: Virology Journal 2018 15 :13
Published on: 15 January 2018
Molecular subtyping of European swine influenza viruses and scaling to high-throughput analysis
Swine influenza is a respiratory infection of pigs that may have a significant economic impact in affected herds and pose a threat to the human population since swine influenza A viruses (swIAVs) are zoonotic .
Authors: Emilie Bonin, Stéphane Quéguiner, Cédric Woudstra, Stéphane Gorin, Nicolas Barbier, Timm C. Harder, Patrick Fach, Séverine Hervé and Gaëlle Simon
Citation: Virology Journal 2018 15 :7
Published on: 10 January 2018
Bacterial ribonuclease binase exerts an intra-cellular anti-viral mode of action targeting viral RNAs in influenza a virus-infected MDCK-II cells
Influenza is a severe contagious disease especially in children, elderly and immunocompromised patients. Beside vaccination, the discovery of new anti-viral agents represents an important strategy to encounter.
Authors: Raihan Shah Mahmud, Ahmed Mostafa, Christin Müller, Pumaree Kanrai, Vera Ulyanova, Yulia Sokurenko, Julia Dzieciolowski, Irina Kuznetsova, Olga Ilinskaya and Stephan Pleschka
Citation: Virology Journal 2018 15 :5
Published on: 5 January 2018
Single-walled carbon nanotubes modulate pulmonary immune responses and increase pandemic influenza a virus titers in mice
Numerous toxicological studies have focused on injury caused by exposure to single types of nanoparticles, but few have investigated how such exposures impact a host’s immune response to pathogen challenge. Fe.
Authors: Hao Chen, Xiao Zheng, Justine Nicholas, Sara T. Humes, Julia C. Loeb, Sarah E. Robinson, Joseph H. Bisesi Jr, Dipesh Das, Navid B. Saleh, William L. Castleman, John A. Lednicky and Tara Sabo-Attwood
Citation: Virology Journal 2017 14 :242
Published on: 22 December 2017
Association of IFITM3 rs12252 polymorphisms, BMI, diabetes, and hypercholesterolemia with mild flu in an Iranian population
IFITM3 has been suggested to be associated with infection in some ethnic groups. Diabetes and hypercholesterolemia are also important clinical conditions that can predispose individual.
Authors: Parvaneh Mehrbod, Sana Eybpoosh, Fatemeh Fotouhi, Hadiseh Shokouhi Targhi, Vahideh Mazaheri and Behrokh Farahmand
Citation: Virology Journal 2017 14 :218
Published on: 9 November 2017
Investigation of antiviral state mediated by interferon-inducible transmembrane protein 1 induced by H9N2 virus and inactivated viral particle in human endothelial cells
Endothelial cells are believed to play an important role in response to virus infection. Our previous microarray analysis showed that H9N2 virus infection and inactivated viral particle inoculation increased t.
Authors: Bo Feng, Lihong Zhao, Wei Wang, Jianfang Wang, Hongyan Wang, Huiqin Duan, Jianjun Zhang and Jian Qiao
Citation: Virology Journal 2017 14 :213
Published on: 3 November 2017
Characteristics of influenza H13N8 subtype virus firstly isolated from Qinghai Lake Region, China
Since the highly pathogenic H5N1 influenza caused thousands of deaths of wild bird in this area in 2005, Qinghai Lake in China has become a hot spot for study of the influence of avian influenza to migratory w.
Authors: Jie Dong, Hong Bo, Ye Zhang, Libo Dong, Shumei Zou, Weijuan Huang, Jia Liu, Dayan Wang and Yuelong Shu
Citation: Virology Journal 2017 14 :180
Published on: 18 September 2017
Effective usage of cationic derivatives of polyprenols as carriers of DNA vaccines against influenza virus
Cationic derivatives of polyprenols (trimethylpolyprenylammonium iodides – PTAI) with variable chain length between 6 and 15 isoprene units prepared from naturally occurring poly-cis-prenols were tested as DNA va.
Authors: Anna Stachyra, Monika Rak, Patrycja Redkiewicz, Zbigniew Madeja, Katarzyna Gawarecka, Tadeusz Chojnacki, Ewa Świeżewska, Marek Masnyk, Marek Chmielewski, Agnieszka Sirko and Anna Góra-Sochacka
Citation: Virology Journal 2017 14 :168
Published on: 2 September 2017
Rapid evolution of the PB1-F2 virulence protein expressed by human seasonal H3N2 influenza viruses reduces inflammatory responses to infection
Influenza A virus (IAV) PB1-F2 protein has been linked to viral virulence. Strains of the H3N2 subtype historically express full-length PB1-F2 proteins but during the 2010–2011 influenza seasons, nearly half o.
Authors: Julie McAuley, Yi-Mo Deng, Brad Gilbertson, Charley Mackenzie-Kludas, Ian Barr and Lorena Brown
Citation: Virology Journal 2017 14 :162
Content type: Short Report
Published on: 22 August 2017
Unexpected complexity in the interference activity of a cloned influenza defective interfering RNA
Defective interfering (DI) viruses are natural antivirals made by nearly all viruses. They have a highly deleted genome (thus being non-infectious) and interfere with the replication of genetically related inf.
Authors: Bo Meng, Kirsten Bentley, Anthony C. Marriott, Paul D. Scott, Nigel J. Dimmock and Andrew J. Easton
Citation: Virology Journal 2017 14 :138
Published on: 24 July 2017
Real-time reverse transcription PCR-based sequencing-independent pathotyping of Eurasian avian influenza A viruses of subtype H7
Low pathogenic avian influenza viruses (LPAIV) of the subtypes H5 and H7 are known to give rise to highly pathogenic (HP) phenotypes by spontaneous insertional mutations which convert a monobasic trypsin-sensi.
Authors: Annika Graaf, Martin Beer and Timm Harder
Citation: Virology Journal 2017 14 :137
Content type: Short report
Published on: 24 July 2017
Avian influenza H9N2 virus isolated from air samples in LPMs in Jiangxi, China
Recently, avian influenza virus has caused repeated worldwide outbreaks in humans. Live Poultry Markets (LPMs) play an important role in the circulation and reassortment of novel Avian Influenza Virus (AIVs). .
Authors: Xiaoxu Zeng, Mingbin Liu, Heng Zhang, Jingwen Wu, Xiang Zhao, Wenbing Chen, Lei Yang, Fenglan He, Guoyin Fan, Dayan Wang, Haiying Chen and Yuelong Shu
Citation: Virology Journal 2017 14 :136
Published on: 24 July 2017
Semi-quantitative Influenza A population averages from a multiplex respiratory viral panel (RVP): potential for reflecting target sequence changes affecting the assay
Yearly influenza virus mutations potentially affect the performance of molecular assays, if nucleic acid changes involve the sequences in the assay. Because individual patient viral loads depend on variables s.
Authors: Kenneth H. Rand, Maura Pieretti, Rodney Arcenas, Stacy G. Beal, Herbert Houck, Emma Boslet and John A. Lednicky
Citation: Virology Journal 2017 14 :128
Published on: 14 July 2017
Maternal antibodies protect offspring from severe influenza infection and do not lead to detectable interference with subsequent offspring immunization
Various studies have shown that infants under the age of 6 months are especially vulnerable for complications due to influenza. Currently there are no vaccines licensed for use in this age group. Vaccination o.
Authors: Joan E. M. van der Lubbe, Jessica Vreugdenhil, Sarra Damman, Joost Vaneman, Jaco Klap, Jaap Goudsmit, Katarina Radošević and Ramon Roozendaal
Citation: Virology Journal 2017 14 :123
Published on: 26 June 2017
Chorioallantoic membranes of embryonated chicken eggs as an alternative system for isolation of equine influenza virus
Influenza virus isolation in embryonated chicken eggs (ECEs) is not applicable for rapid diagnosis, however it allows the recovery and propagation of the viable virus. A low number of infectious virus particle.
Authors: Ilona Marcelina Gora, Malgorzata Kwasnik, Jan Franciszek Zmudzinski and Wojciech Rozek
Citation: Virology Journal 2017 14 :120
Content type: Short Report
Published on: 21 June 2017
Identification of Two novel reassortant avian influenza a (H5N6) viruses in whooper swans in Korea, 2016
On November 20, 2016 two novel strains of H5N6 highly pathogenic avian influenza virus (HPAIVs) were isolated from three whooper swans (Cygnus cygnus) at Gangjin Bay in South Jeolla province, South Korea. Identif.
Authors: Jipseol Jeong, Chanjin Woo, Hon S. Ip, Injung An, Youngsik Kim, Kwanghee Lee, Seong-Deok Jo, Kidong Son, Saemi Lee, Jae-Ku Oem, Seung-Jun Wang, Yongkwan Kim, Jeonghwa Shin, Jonathan Sleeman and Weonhwa Jheong
Citation: Virology Journal 2017 14 :60
Content type: Short report
Published on: 21 March 2017
A novel benzo-heterocyclic amine derivative N30 inhibits influenza virus replication by depression of Inosine-5’-Monophospate Dehydrogenase activity
Influenza virus is still a huge threat to the world-wide public health. Host inosine-5’- monophosphate dehydrogenase (IMPDH) involved in the synthesis of guanine nucleotides, is known to be a potential target .
Authors: Jin Hu, Linlin Ma, Huiqiang Wang, Haiyan Yan, Dajun Zhang, Zhuorong Li, Jiandong Jiang and Yuhuan Li
Citation: Virology Journal 2017 14 :55
Published on: 15 March 2017
Surveillance of avian influenza viruses in South Korea between 2012 and 2014
National surveillance of avian influenza virus (AIV) in South Korea has been annually conducted for the early detection of AIV and responses to the introduction of highly pathogenic avian influenza (HPAI) viru.
Authors: Eun-Kyoung Lee, Hyun-Mi Kang, Byung-Min Song, Yu-NA Lee, Gyeong-Beum Heo, Hee-Soo Lee, Youn-Jeong Lee and Jae-Hong Kim
Citation: Virology Journal 2017 14 :54
Content type: Research article
Published on: 14 March 2017
Isolation and genetic characterization of a novel 22.214.171.124a H5N1 virus from a vaccinated meat-turkeys flock in Egypt
Vaccination of poultry to control highly pathogenic avian influenza virus (HPAIV) H5N1 is used in several countries. HPAIV H5N1 of clade 2.2.1 which is endemic in Egypt has diversified into two genetic clades.
Authors: Ahmed H. Salaheldin, Jutta Veits, Hatem S. Abd El-Hamid, Timm C. Harder, Davud Devrishov, Thomas C. Mettenleiter, Hafez M. Hafez and Elsayed M. Abdelwhab
Citation: Virology Journal 2017 14 :48
Published on: 9 March 2017
The intranasal adjuvant Endocine™ enhances both systemic and mucosal immune responses in aged mice immunized with influenza antigen
Despite availability of annual influenza vaccines, influenza causes significant morbidity and mortality in the elderly. This is at least in part a result of immunosenescence the age-dependent decrease in immu.
Authors: Tina Falkeborn, Jorma Hinkula, Marie Olliver, Alf Lindberg and Anna-Karin Maltais
Citation: Virology Journal 2017 14 :44
Content type: Short report
Published on: 3 March 2017
New H6 influenza virus reassortment strains isolated from Anser fabalis in Anhui Province, China
H6 subtype avian influenza viruses are globally distributed and, in recent years, have been isolated with increasing frequency from both domestic and wild bird species as well as infected humans. Many reports .
Authors: Ye Ge, Hongliang Chai, Zhiqiang Fan, Xianfu Wang, Qiucheng Yao, Jian Ma, Si Chen, Yuping Hua, Guohua Deng and Hualan Chen
Citation: Virology Journal 2017 14 :36
Published on: 21 February 2017
Identification of influenza A nucleoprotein body domain residues essential for viral RNA expression expose antiviral target
Influenza A virus is controlled with yearly vaccination while emerging global pandemics are kept at bay with antiviral medications. Unfortunately, influenza A viruses have emerged resistance to approved influe.
Authors: Alicia M. Davis, Jose Ramirez and Laura L. Newcomb
Citation: Virology Journal 2017 14 :22
Published on: 7 February 2017
The potential influence of human parainfluenza viruses detected during hospitalization among critically ill patients in Kuwait, 2013–2015
The four types of human parainfluenza viruses (PIV) are important causes of community-acquired pneumonia, particularly in children however, limited information exists about the incidence of PIV in critically .
Authors: Sahar Essa, Haya Al-tawalah, Sarah AlShamali and Widad Al-Nakib
Citation: Virology Journal 2017 14 :19
Published on: 3 February 2017
Host Cell Copper Transporters CTR1 and ATP7A are important for Influenza A virus replication
The essential role of copper in eukaryotic cellular physiology is known, but has not been recognized as important in the context of influenza A virus infection. In this study, we investigated the effect of cel.
Authors: Jonathan C. Rupp, Manon Locatelli, Alexis Grieser, Andrea Ramos, Patricia J. Campbell, Hong Yi, John Steel, Jason L. Burkhead and Eric Bortz
Citation: Virology Journal 2017 14 :11
Published on: 23 January 2017
Effects of calcitriol (1, 25-dihydroxy-vitamin D3) on the inflammatory response induced by H9N2 influenza virus infection in human lung A549 epithelial cells and in mice
H9N2 influenza viruses circulate globally and are considered to have pandemic potential. The hyper-inflammatory response elicited by these viruses is thought to contribute to disease severity. Calcitriol plays.
Authors: Boxiang Gui, Qin Chen, Chuanxia Hu, Caihui Zhu and Guimei He
Citation: Virology Journal 2017 14 :10
Published on: 23 January 2017
Amino acid substitutions involved in the adaptation of a novel highly pathogenic H5N2 avian influenza virus in mice
H5N2 avian influenza viruses (AIVs) can infect individuals that are in frequent contact with infected birds. In 2013, we isolated a novel reassortant highly pathogenic H5N2 AIV strain [A/duck/Zhejiang/6DK19/20.
Authors: Haibo Wu, Xiuming Peng, Xiaorong Peng and Nanping Wu
Citation: Virology Journal 2016 13 :159
Content type: Short report
Published on: 23 September 2016
Codon optimization of antigen coding sequences improves the immune potential of DNA vaccines against avian influenza virus H5N1 in mice and chickens
Highly pathogenic avian influenza viruses are a serious threat to domestic poultry and can be a source of new human pandemic and annual influenza strains. Vaccination is the main strategy of protection against.
Authors: Anna Stachyra, Patrycja Redkiewicz, Piotr Kosson, Anna Protasiuk, Anna Góra-Sochacka, Grzegorz Kudla and Agnieszka Sirko
Citation: Virology Journal 2016 13 :143
Published on: 26 August 2016
First outbreaks and phylogenetic analyses of avian influenza H9N2 viruses isolated from poultry flocks in Morocco
H9N2 avian influenza viruses continue to spread in poultry and wild birds worldwide. Morocco just faced its first H9N2 influenza virus outbreaks early 2016 affecting different types of poultry production. Afte.
Authors: Mohammed EL Houadfi, Siham Fellahi, Saadia Nassik, Jean-Luc Guérin and Mariette F. Ducatez
Citation: Virology Journal 2016 13 :140
Published on: 15 August 2016
G45R mutation in the nonstructural protein 1 of A/Puerto Rico/8/1934 (H1N1) enhances viral replication independent of dsRNA-binding activity and type I interferon biology
The nonstructural protein 1 (NS1) of influenza A viruses can act as a viral replication enhancer by antagonizing type I interferon (IFN) induction and response in infected cells. We previously reported that A/.
Authors: Challika Kaewborisuth, Mark Zanin, Hans Häcker, Richard J. Webby and Porntippa Lekcharoensuk
Citation: Virology Journal 2016 13 :127
Published on: 12 July 2016
Evaluation of custom multiplex real - time RT - PCR in comparison to fast - track diagnostics respiratory 21 pathogens kit for detection of multiple respiratory viruses
Severe acute respiratory infections in children can be fatal, rapid identification of the causative agent and timely treatment can be life saving. Multiplex real time RT-PCR helps in simultaneous detection of .
Authors: Bharti Malhotra, M. Anjaneya Swamy, P. V. Janardhan Reddy, Neeraj Kumar and Jitendra Kumar Tiwari
Citation: Virology Journal 2016 13 :91
Expression of importin-α isoforms in human nasal mucosa: implication for adaptation of avian influenza A viruses to human host
Transportation into the host cell nucleus is crucial for replication and transcription of influenza virus. The classical nuclear import is regulated by specific cellular factor, importin-α. Seven isoforms of i.
Authors: Khwansiri Ninpan, Ornpreya Suptawiwat, Chompunuch Boonarkart, Peerayuht Phuangphung, Sakda Sathirareuangchai, Mongkol Uiprasertkul and Prasert Auewarakul
Citation: Virology Journal 2016 13 :90
Content type: Short report
Pre-immune state induced by chicken interferon gamma inhibits the replication of H1N1 human and H9N2 avian influenza viruses in chicken embryo fibroblasts
Interferon gamma (IFN-γ), an immunoregulatory cytokine, is known to control many microbial infections. In a previous study, chicken interferon gamma (chIFN-γ) was found to be up-regulated following avian influ.
Authors: Seong-Su Yuk, Dong-Hun Lee, Jae-Keun Park, Erdene-Ochir Tseren-Ochir, Jung-Hoon Kwon, Jin-Yong Noh, Joong-Bok Lee, Seung-Yong Park, In-Soo Choi and Chang-Seon Song
Citation: Virology Journal 2016 13 :71
Published on: 27 April 2016
A heat-inactivated H7N3 vaccine induces cross-reactive cellular immunity in HLA-A2.1 transgenic mice
Cross-reactive immunity against heterologous strains of influenza virus has the potential to provide partial protection in individuals that lack the proper neutralizing antibodies. In particular, the boosting .
Authors: Giuseppina Di Mario, Bruno Garulli, Ester Sciaraffia, Marzia Facchini, Isabella Donatelli and Maria R. Castrucci
Citation: Virology Journal 2016 13 :56
Published on: 31 March 2016
Surveillance for Eurasian-origin and intercontinental reassortant highly pathogenic influenza A viruses in Alaska, spring and summer 2015
Eurasian-origin and intercontinental reassortant highly pathogenic (HP) influenza A viruses (IAVs) were first detected in North America in wild, captive, and domestic birds during November–December 2014. Detec.
Authors: Andrew M. Ramey, John M. Pearce, Andrew B. Reeves, Rebecca L. Poulson, Jennifer Dobson, Brian Lefferts, Kyle Spragens and David E. Stallknecht
Citation: Virology Journal 2016 13 :55
Content type: Short report
Published on: 31 March 2016
Phylodynamics of avian influenza clade 2.2.1 H5N1 viruses in Egypt
Highly pathogenic avian influenza (HPAI) viruses of the H5N1 subtype are widely distributed within poultry populations in Egypt and have caused multiple human infections. Linking the epidemiological and sequen.
Authors: Abdelsatar Arafa, Ihab El-Masry, Shereen Kholosy, Mohammed K. Hassan, Gwenaelle Dauphin, Juan Lubroth and Yilma J. Makonnen
Citation: Virology Journal 2016 13 :49
Published on: 22 March 2016
Characterisation of the epidemic strain of H3N8 equine influenza virus responsible for outbreaks in South America in 2012
An extensive outbreak of equine influenza occurred across multiple countries in South America during 2012. The epidemic was first reported in Chile then spread to Brazil, Uruguay and Argentina, where both vacc.
Authors: Edsel Alves Beuttemmüller, Alana Woodward, Adam Rash, Luis Eduardo dos Santos Ferraz, Alice Fernandes Alfieri, Amauri Alcindo Alfieri and Debra Elton
Citation: Virology Journal 2016 13 :45
Published on: 19 March 2016
Human H7N9 virus induces a more pronounced pro-inflammatory cytokine but an attenuated interferon response in human bronchial epithelial cells when compared with an epidemiologically-linked chicken H7N9 virus
Avian influenza virus H7N9 has jumped species barrier, causing sporadic human infections since 2013. We have previously isolated an H7N9 virus from a patient, and an H7N9 virus from a chicken in a live poultry.
Authors: Kelvin K. W. To, Candy C. Y. Lau, Patrick C. Y. Woo, Susanna K. P. Lau, Jasper F. W. Chan, Kwok-Hung Chan, Anna J. X. Zhang, Honglin Chen and Kwok-Yung Yuen
Citation: Virology Journal 2016 13 :42
Published on: 15 March 2016
Lst1 deficiency has a minor impact on course and outcome of the host response to influenza A H1N1 infections in mice
Previously, we performed a quantitative trait locus (QTL) mapping study in BXD recombinant inbred mice to identify host genetic factors that confer resistance to influenza A virus infection. We found Lst1 (leukoc.
Authors: Sarah R. Leist, Heike Kollmus, Bastian Hatesuer, Ruth L. O. Lambertz and Klaus Schughart
Citation: Virology Journal 2016 13 :17
Content type: Short report
Published on: 27 January 2016
Serological evidence of H9N2 avian influenza virus exposure among poultry workers from Fars province of Iran
Since the 1990s, influenza A viruses of the H9N2 subtype have been causing infections in the poultry population around the globe. This influenza subtype is widely circulating in poultry and human cases of AI H.
Authors: A. Heidari, M. Mancin, H. Nili, G. H. Pourghanbari, K. B. Lankarani, S. Leardini, G. Cattoli, I. Monne and A. Piccirillo
Citation: Virology Journal 2016 13 :16
Published on: 27 January 2016
Prevalence of gastrointestinal symptoms in patients with influenza, clinical significance, and pathophysiology of human influenza viruses in faecal samples: what do we know?
This review provides for the first time an assessment of the current understanding about the occurrence and the clinical significance of gastrointestinal (GI) symptoms in influenza patients, and their correlat.
Authors: Laetitia Minodier, Remi N. Charrel, Pierre-Emmanuel Ceccaldi, Sylvie van der Werf, Thierry Blanchon, Thomas Hanslik and Alessandra Falchi
Citation: Virology Journal 2015 12 :215
Published on: 12 December 2015
Matrix-M™ adjuvation broadens protection induced by seasonal trivalent virosomal influenza vaccine
Influenza virus infections are responsible for significant morbidity worldwide and therefore it remains a high priority to develop more broadly protective vaccines. Adjuvation of current seasonal influenza vac.
Authors: Freek Cox, Eirikur Saeland, Matthijs Baart, Martin Koldijk, Jeroen Tolboom, Liesbeth Dekking, Wouter Koudstaal, Karin Lövgren Bengtsson, Jaap Goudsmit and Katarina Radošević